2. • Introduction
• Epidemiology
• Clinical features and classification
• KUTB and GUTB
• Diagnosis
• Culture
• Imaging
• Urethrocystoscopy
• Treatment
• Medical
• Surgical
Genitourinary TB(Ibsa.D) 2
3. Epidemiology
• WHO 2013 – quarter world’s population is infected with MTBC in its latent form.
• Second great imitator after syphilis
• In developing countries 90 % of GUTB occurs and
• 15% to 20% with pulmonary TB
• the GU tract is the second most common extra pulmonary site after lymph
nodes
• In developed countries, GU TB has been found 27% of extrapulmonary cases.
• USA GU TB is the third most common form after pleural and lymphatic TB
• 2-10 of cases with pulmonary TB
• Male to female ratio(2:1)
• Mean age of affection is 40 years
Genitourinary TB(Ibsa.D) 3
4. Pathogenesis
• Latent TB is marked by cicatrization and
granuloma calcification.
• In fewer than 5% of primary progression
• Lifetime risk of reactivation TB is
estimated at 5% to 15%.
• the risk is higher in patients with the
medical comorbidities
Genitourinary TB(Ibsa.D) 4
5. GUTB development
• 1.Hematogenous spread-
• principal route
• active or latency
• 2.Ascending/retrograde infection
• Second route of infection
• BCG for treatment of Bladder cancer in 0.9%
• 3.Contiguous spread
• Extension from spine and
psoas
• Entero renal and entero
vesical fistula
• 4.Direct inoculation
• Very rare
Genitourinary TB(Ibsa.D) 5
6. Clinical features and classification
• Nonspecific sign and symptoms.
• 8.4% of GU TB patients are
asymptomatic
• The typical TB constitutional symptoms
of present in less than 20% of patients
• 50% of only dysuria
• 50% have storage symptoms
• 33% have hematuria and
• Renal colicky in 10%
• Typical laboratory findings include
sterile pyuria and/or hematuria is
found in more than 90% of GU TB
patients in developing countries
Genitourinary TB(Ibsa.D) 6
7. Clinical Classification of Urogenital Tuberculosis
kidney ( GUTB) nephron tuberculosis(Kulchavenya, 2014)
• KTB 1)
• TB of kidney parenchyma
• Occasional dx
• Nondestructive form is subject to
conservative therapy.
• CTX ( anti TB)
• KTB 2
• Small-destructive form
is subject to conservative therapy,
• Reconstructive surgery is indicated
for complications only.
• Unilateral or bilateral
• Solitary or multiple
KTB 3
• From parenchyma or papillitis
• Cavernous( subcortical cavern is like renal
carbuncle
• Poly-cavernous KTB and destruction from papiltis
• surgery indicated
• KTB 4
• Widespread destructive form recovery with anti-TB
drugs only is impossible,
• surgery is necessary, basically nephrectomy
•
Genitourinary TB(Ibsa.D) 7
8. 2.UTTB (urinary tract tuberculosis)
• TB of pelvis, ureters, bladder, and
urethra.
• Always secondary to KTB.
• Usually develops in the lower third
of ureter ,
• Strictures can also occur throughout
the ureter in a “pan-ureteral” fashion
leading to a “beaded corkscrew”
appearance.
• Urinary obstruction resulting from
strictures is an important cause of
renal failure in GU TB
Genitourinary TB(Ibsa.D) 8
9. Bladder
• Usually begins near the ureteral
orifices
• Implant in the urothelium and
cause a patchy cystitis.
• The dome of the bladder is the
most affected,
• whereas the trigone and neck usually
remain normal
• chronic inflammation and mucosal
scarring, bladder contracture develops
• Urinary frequency, urgency, pain, and
dysuria become prominent when bladder
capacity shrinks to less than 100 mL.
• The severely contracted “thimble”
bladder typically has a capacity of less
than 20 mL .
Genitourinary TB(Ibsa.D) 9
10. Kulchavenya, Divided bladder Tb in to 4 stages
• Stage 1- Tubercle infiltrative
• Stage 2- Erosive ulcerous
• Stage 3- Spastic cystitis
(bladder contraction , false
microcystitis) overactive bladder.
• Stage 4- Real microcytitis up to full
obliteration.
• The first two stages should be
treated by standard
anti-TB drugs,
• The third stage with standard
anti TB drugs and trospium
chloride.
• The fourth stage is indicated for
cystectomy with following
enteroplasty.
Genitourinary TB(Ibsa.D) 10
11. II. MGTB(male genital tuberculosis)
• TB epididymitis
• Unilateral ,can be bilateral in
34%
• Second most common site of
hematogenous seeding
• More affects the more
vascular globus minor
• Ulceration and tuberculous
sinus tract in 50 %
• Prostate TB (infiltrative or cavernous
forms);
• Hematogenous
• periphery and spare urethra
• Calcification and gland
hardening
• Urinary tract
• More affects the urethra and
manifests like bacterial
prostatitis
• Prostatic abscess in AIDS
patients
Genitourinary TB(Ibsa.D) 11
12. TB of seminal vesicles
• Cause of infertility
• Through urethra and also ejaculatory ducts
• Granulomas and further calcification
• Oligospermia,
• Azoospermia,
• Hematospermia.
• TB can rarely cause seminal vesicle abscesses
Genitourinary TB(Ibsa.D) 12
13. Penis and Urethra
• Involved in only 1.9% to 4.5% of GU TB
patients.
• Isolated urethral TB is very rare but has
been reported
• Urethral TB is usually associated with
prostate infection and complicated with
urethra cutaneous fistula (watering
pot perineum)
• Penile lesions begin on the skin as an
inflamed papule or a keratotic plaque (also
known as lupus vulgaris)
• ulcerate and spread to cavernous tissue
• these can be hard and mimicks malignancy and if
there is fibrosis penis can be distorted
Genitourinary TB(Ibsa.D) 13
14. •
Diagnosis
1.Culture
• Gold standard for the diagnosis of GU TB is urine acid fast bacilli (AFB)
culture.
• First-void urine is the best sample
• 3-5 urine samples on consecutive days
• The sensitivity is as high as 80% when done in this manner.
Genitourinary TB(Ibsa.D) 14
15. Cont …
• LJ (Lowenstein jansen) medium -Traditionally on solid , egg based
• Laborious and time consuming 4 to 6 weeks
• Middlebrook 7H10- Developed world in solid agar, based medium,
• Liquid based (BACTEC mycobacteria growth indicator tube (MGIT)
• Flouresence method detect MTB in as little as 10 days
• Current guidelines recommend culturing on at least one solid medium
concurrently with the liquid system to maximize yield
• ATB sensitivity to firsts line and second line can also be done
Genitourinary TB(Ibsa.D) 15
16. 2. NEUCLIC ACID AMPLIFICATION TESTS
• Providing results in 1 to 2 days
• Can detect in low bacillary load
• Sensitivity ranges from 87% to 96%
• Lower in non sputum specimens
• Urine contains natural inhibitors that interfere with DNA/RNA amplification
• 2010,WHO enthusiastically endorsed the newest TB PCR assay on the
market, the Gene-xpert MTB/RIF
• In small study EPTB 91 urine samples ( only 5 were culture positive) and
Gene expert was 100% sensitive and 98.6% specific
Genitourinary TB(Ibsa.D) 16
17. 3.Histopathology
• Caseating granulomas
• In patients with epididymal
nodules, fine-needle aspiration
cytology can provide a
diagnosis in 67.5% .
• Adding NAAT can further
augment diagnostic sensitivity to
tissue specimens
Genitourinary TB(Ibsa.D) 17
18. 4.Radiography
• GU TB generates a wide
spectrum of imaging findings.
• The test of choice depends on
disease location and should be
driven by symptoms and other
clinical data.
• Imaging is often the first test
that indicates TB is the cause
of a GU disorder
• Plain radiography
• IVU
• Retrograde pyelography
• Ultrasonography
• CT scan
• MRI
Genitourinary TB(Ibsa.D) 18
19. Plain radiography
• Calcifications- 50%
• Lobar pattern -pathognomonic
• Globular calcifications
• Triangular ring like calcifications for
papillary necrosis
• Cement or putty kidney: the calcific
rim outlines the renal lobes
• Renal and ureteral TB-infected
stones
• Kerr’s kink
• Bladder wall calcification
Genitourinary TB(Ibsa.D) 19
20. Intravenous urography
• GOLD standard in imaging
of early renal TB
• Loss of sharpness and
edge irregularities
• Calyceal erosions have a
‘Moth-eaten’ appearance
• Filling defect by
tuberculomas
• Phantom calyx
• Rigid, calcified,
straightened, pipestem
ureter
• Beaded corkscrew ureter
• Hiked up pelvis
• Obstructive changes
• Cloverleaf pattern,
calyceal dilation and
distortion
• Calyceal distortion
• Infindibular
narrowing
• Hydrocalycosis
• hydroureter
Genitourinary TB(Ibsa.D) 20
22. CT urography scan
• Replaced IVP
• Calcifications, scarring and signs of
obstruction
• Useful in evaluating patients with
complicated and extensive TB
• Les sensitive for detecting urothelial
thickening and subtle papillary necrosis
for which IVU is still preferred
• High dose of radiation
Genitourinary TB(Ibsa.D) 22
24. Ultrasonography
• Limited use in diagnosing GU
TB
• Primary use of US is for
following Hydronephrosis in
patients who are receiving
medical treatment
• fibrosis during healing can worsen
obstruction
• Pediatrics and pregnant
• Evaluate the testis, epididymis,
seminal vesicles,
• locate abscess and cavities
• Presence of ascites,LAP or omental
caking
Genitourinary TB(Ibsa.D) 24
25. Retrograde pyelography
• Replaced by CTU
• However when CT cannot be
done because of renal
insufficiency or contrast allergy,
• In addition can be used with IVU
to determine cavitation's are
obstructive or nonobstructive
• Useful in pediatric and pregnant
patients
• Sensitive than IVU in showing
caliectasis and urothelial thickingin
• DWI helps In distinguishing
pyonephrosis from HN
• MRU ureteral peristalisis
MRI
Genitourinary TB(Ibsa.D) 25
26. 5.Cytoscopy and
ureteroscopy
• Limited role Findings are
nonspecific
• Local hyperemia,
• Mucosal erosion,
• Ulceration,
• Granulomatous masses,
• Irrhole UO
• egularity of UO
• Golf
Genitourinary TB(Ibsa.D) 26
27. Treatment
• Medical therapy
• Combination therapy with first line ATDs
• Second line agents are reserved for
• Failed first line agents
• Side effects of first line agents
• Drug resistance for first line agents
• Treatment should start with these—namely, INH, rifampin, pyrazinamide, and
ethambutol.
• Before the start of treatment, baseline measurements should include blood
counts and liver and kidney function tests
Genitourinary TB(Ibsa.D) 27
28. Cont….
• Intensive phase(2 months): targeting for rapidly multiplying bacteria
• Continuation phase(6 months): to eradicate slow, sporadic multipliers
and persistent bacteria
• The role of steroid used in GUTB to prevent ureteral strictures and
bladder contraction,
• these are anecdotal and no clinical trials are further conducted
Genitourinary TB(Ibsa.D) 28
29. Duration of therapy
• Usually 6 months of standard short course therapy
• 9 months therapy is indicated in:
• Extensive pockets of infection
• Concurrent smear positive cavitary pulmonary disease
• CNS involvement
• Delay in positive cultures converting to negative
• If the patient is not taking Pyrazinamide for at least 2 months
• Some clinicians recommend treatment with 12 months of therapy
because of high relapse rates of 22% if given only for 6 months
29
Genitourinary TB(Ibsa.D)
30. • Surgical therapy
Optimal therapy for surgery is 4-6 weeks after initiation of ATDs
Operative management can be categorized in seven groups
1.Drainage for hydronephrosis (stenting or PCN insertion)1
2.Drainage for abscesses and caverns
3.Definitive local treatment of kidney tuberculosis(partial nephrectomy)
4.Reconstruction of upper UT
(calico/pyeloureterostomy, ureterolysis, ureterocystoneostomy, ureter
replacement)
5.Bladder augmentation
6.Reconstruction of urethra
7.Management of genital tuberculosis (epidiymorchidectomy)
Genitourinary TB(Ibsa.D) 30
31. 1. Drainage for hydronephrosis (stenting or PCN insertion)
• Should be done soon in uremia and
sepsis
• Stenting, reassess after 6 weeks
• Percutaneous
nephrostomy(PCN)
• Stenting retrograde is successful
in 41%
• If that fails antegrade stenting via
PCN
• PCN should be performed.
• Risk of tuberculous cutaneous
fistula during PCN removal.
• Avoid high contrast injection
pressures during stent or PCN
Genitourinary TB(Ibsa.D) 31
32. 2. Drainage for abscesses and caverns
• In septic cases drainage of the caverns of the kidney may be
necessary.
• Open surgical drainage of an abscess should not be attempted.
• The contents of an abscess should be aspirated in a minimally invasive
manner
Genitourinary TB(Ibsa.D) 32
33. 3. Definitive local treatment of kidney tuberculosis
• Nephrectomy indications
1.Nonfunctional kidney and recalcitrant
or recurrent TB despite optimal medical
therapy.
2. Nonfunctional kidney and medically
resistant hypertension.
• Partial nephrectomy indications
1. Localized polar lesion that failed to
respond to intensive CTX after 6 weeks
2.Area of calcification that is slowly
increasing in size and threatening to
destroy the whole kidney.
Genitourinary TB(Ibsa.D) 33
34. 4. Reconstruction of upper UT
Endoscopically or Open surgery
• Endoscopic management
• Upper and mid ureteric stricture
• Temporarily stenting for UPJ strictures
• Balloon dilation retrograde and antegrade access for UPJ,UVK and calyceal
infindibula
• Follow up needed
• High failure rates
• Steroid can be added
• If no improvement after 6 weeks open surgical treatment required
Genitourinary TB(Ibsa.D) 34
35. Open approach
• Dismembered pyeloplasty for
extrarenal pelvis
• Nondismebered pyeloplasty for
longer strictures but not feasible
because of excessive scarring
• Ureterocalicostomy (ureter to
lower pole of calyx)
• Upper and mid ureter- tension
free ureteroureterostomy
• Lower ureteric stricture-
ureteroneocystomy
• Psoas hitch— < 5cm
• Boari flap- 10 cm
• Ileal interposition in multiple
and recurrent strictures
Genitourinary TB(Ibsa.D) 35
36. 5.Bladder augmentation
1.Augmentation cystoplasty
(ileocecum or sigmoid segments
are most suitable)
• Indicated when frequency,
nocturia, urgency and pain and
hematuria intolerable
• Bladder capacity <100ml
• 2.Thimble bladder with <20ml
capacity best managed by
• orthotopic bladder substation
Genitourinary TB(Ibsa.D) 36
37. 6.Reconstruction of urethra
• Bladder neck contracture -transurethral incision of contracture
• Urethral strictures --endoscopically
• often require repeated procedures.
• Tuberculous urethral fistulae are treated by initiation of medical
therapy and suprapubic bladder drainage
• Delayed reconstruction is preferred
Genitourinary TB(Ibsa.D) 37
38. 7.Management of genital tuberculosis (epidiym orchidectomy)
• Extirpative surgery for genital TB is considered only for patients in
whom medical therapy has failed.
• When epididymis infected sparing the testis, every effort should be
performed to do epidymectomy without orchidecotmy
• If testis infected scrotal orchidecotmy can be done
• Involvement of the vas deferens by TB is usually distal to the external
ring and ligation of at the level of the ring is possible and sufficient.
Genitourinary TB(Ibsa.D) 38
40. 2.Articles and journals
1.Lenk S, Naber KG, Bishop MC, Johansen TEB, Botto H, Grabe M, et al. European Urology EAU Guidelines
for the Management of Genitourinary Tuberculosis Mete C. 2005;48:353–62.
2. Abbara A, Davidson RN. Etiology and management of genitourinary tuberculosis. Nat Rev Urol
[Internet]. 2011;8(12):678–88. Available from: http://dx.doi.org/10.1038/nrurol.2011.172
3. Çalışkan S. SM Gr up Diagnosis of Genitourinary Tuberculosis. 2016;1–8.
4. Carl P, Stark L. Indications for Surgical Management of Genitourinary Tuberculosis. 1997;505–10.
5. Kulchavenya E. Urogenital tuberculosis : definition and classification. 2015;1–6.
6. Merchant S, Bharati A, Merchant N. Tuberculosis of the genitourinary system - Urinary tract
tuberculosis : Renal tuberculosis – Part II. 2013;23(1).
7. Dhangar SP, Kothawala IH, Patil S, Kumar A, Whatkar A. Radiologic signs of genitourinary tuberculosis :
An aid for earlier diagnosis. 2016;1(4):1–8.
Genitourinary TB(Ibsa.D) 40
Editor's Notes
Initial mode of entry of MTBC into the host is via inhalation cough-generated infectious aerosols,
direct inoculation of MTBC into soft tissues
Bacilli reach the alveoli, they are phagocytosed by alveolar macrophages.
In some persons, MTBC organisms are killed by the macrophages at this point and effectively cleared
In others, MTBC bacilli escape killing, begin to replicate within macrophages, establish infection
Up to 12 weeks may pass before a cellular immune response is detectable and before this development the tubercle bacilli can spread through the lymphatics to the hilar lymph nodes and ultimately through the bloodstream to seed distant organs.
The two forms of TB described—latent TB infection and active TB disease—representa simplification of what is now understood to be a spectrum; adynamic continuum between contained TB infection, subclinicalTB disease, and progressively infectious TB disease.
Disseminated TB--high numbers of bacilli leads to innumerable small (3-mm), pale clumps of granulomas that look like scattered millet seeds on gross pathologic examination of the kidney
In the kidney, the “milia” can be found studding the renal cortex and medulla and do not usually affect renal function
localized infection of the kidney, tubercle bacilli become lodged first in the periglomerular capillaries.
Granulomas form in the renal parenchyma and coalesce.
When they caseate, cavities with necrotic material form.
result in frank abscesses, chronic pyelonephritis, and parenchymal and papillary necrosis. Sinus tracts may emerge along the flanks
As infection advances, the calyces become inflamed and eventually calcify, resulting in calyceal distortion, dilatation, and stenosis
An individual who has acquired TB can move forward and backward along this spectrum through his or her lifetime, depending on changes in hostimmunity such as imparted by medical comorbidities or changesin the bacilli such as imparted by treatment for latent TB infection
Hematogenous spread-prinicipal route, active or latency
Typical sites for GU seeding are kidneys and epididymis
Other organs of GUT is infected via contiguous spread from these initial landing
Ascending/retrograde infection
Second route of infection
BCG for treatment of Bladder cancer in 0.9
Contiguous spread
Extension from spine and psoas
Entero renal and entero vesical fistula
Direct inoculation
Very rare
Complications of nephrotuberculosis:chronic renal failure, fistula, high blood pressure.
KTB-2 may be unilateral and bilateral, solitary
and multiple. KTB-2 is often complicated by
UTTB. KTB-2 should be treated with anti-TB
drugs; if complicated, reconstructive surgery is
indicated. Prognosis is good, outcome is usually
recovery with fibrous deformation and post-TB
pyelonephritis. With inappropriate therapy KTB
has two routes of pathogenesis: from TB
of parenchyma or from papillitis. The first means
the development of a subcortical cavern without
connection to the collecting system. The clinical
manifestation of a subcortical cavern is like a
renal carbuncle, thus the diagnosis usually is
made after the operation. The second is the progress of the destruction of the papilla until cavern
development. Cavernous KTB may be unilateral
and bilateral, papillitis in one kidney and cavernous TB in another is usual; in this case the patient
should be treated as a patient with KTB-3.
Complications develop in more than half of the
patients. Full recovery by anti-TB drugs is
impossible, surgery is in general indicated. The
benefit outcome is the formation of a sterile cyst;
negative outcome is progress destruction until
polycavernous TB
TB should be suspected in patients with chronic prostatitis that persists despite antibiotics. Quinolones used to treat routine bacterial prostatitis are
also active against MTBC. However, the shorter courses used for
bacterial prostatitis are not sufficient for TB prostatitis, and the
symptoms will not resolve or will quickly recur. Prostatic abscesses
are rare but do occur, particularly in acquired immunodeficiency
syndrome (AIDS) patients
Orificial TB, a rapidly necrotic form of penile TB, has also been reported
It arises from autoinoculation of the penile skin with infected stool or urine from the patient, or rarely from hematogenous or lymphatic spread
Orificial TB is a presentation of very advanced and severe TB elsewhere in the GU or GI tract and carries a poor prognosis
The urethra appears somewhat resistant to TB infection and is involved in only 1.9% to 4.5% of GU TB patients.
It is typically associated with prostate infection and can manifest with urethroscrotal fistulae.
Isolated urethral TB is very rare but has been reported
Urethral TB is usually associated with prostate infection and complicated with urethrocutaneous fistula(watering pot perineum)
Other available detection methods include semiautomated systems
that use radiometric liquid culture. Antibiotic susceptibility can be
tested using any of the culture methods described earlier. Typically,
susceptibility to first-line TB drugs is tested “in house” with use of
the MGIT instrument. Susceptibility testing for second-line TB drugs
is generally performed only at reference laboratories.
Nonsputum specimens urine contain natural inhibitors that interfere with the DNA or RNA amplification process, potentially resulting in false-negative test results.
2010,WHO enthusiastically endorsed the newest TB PCR assay on the market, the gene xpert MTB/RIF
In general, nucleic acid amplification tests (NAATs) are frequently underused in developed countries because culture is necessary for drug susceptibility testing.
In developing countries, the cost
and the need for expensive equipment have been the obstacles.
Unlike cultures, NAATs cannot be used to monitor response to
treatment because nucleic acids are shed from dead organisms and
test results can remain positive despite adequate treatment
Papillary necrosis-triangular calcifications in the collecting system
Fibrotic autonephrectomy -small ,shrunken, calcified cement putty kidney
(calcific rims outline the individual renal is pathognomonic of ESRD) lobes,which
Renal and uretral TB infected calculi.
Stones may take strange shapes as deformed and fibrosed renal pelvis. upward arrowhead ,indicate renal pelvis that has been hiked up by contraction from scarring.
“hiked-up” renal pelvis, with sharp angulation of the ureteropelvic junction (UPJ), is known as “Kerr’s kink”
The IVU has been considered as one of the most useful tests for
obtaining anatomical and functional details of the kidneys [14]. It
can show a broad range of findings, depending on the severity
of infection. In a series of 45 patients, the IVU pointed to the
diagnosis of urinary TB in 88% [15]. However, approximately 10-
15% of patients who present with active renal TB may have
normal urographic findings
The earliest urographic change occurs in the minor calyces, with subtle initial signs such as minimal calyceal dilatation [5] and mild loss of calyceal sharpness due to mucosal edema [17] (Fig 3A,3B). As the disease progresses, the calyceal outline becomes more irregular, fuzzy, and ragged and, later, feathery and moth-eaten in appearance
Medullary cavities that communicate collecting system
Phantom calyx- whne calyx or infidibulum is stenosis,contrast excretion fails and creates
Uretral TB-rigid,calcifies,straightened pipestem uretet that is tubular and lacks peristalitic activity
Obstructive changes
Cloverleaf pattern, calyceal dilation and distortion
Hiked-up renal pelvis(when the pelvis is pulled from scaring) with UPJ kerr’s king(when acute angulation at UPJ)
TB papillary necrosis results
not only from ischemia, which is the basis of change in most
renal papillary necrosis, but also as a result of direct tissue
destruction. We have seen classic early forniceal and even
central papillary necrosis (Fig 3A, 3B) in numerous proven cases
of renal TB that cannot be differentiated from papillary necrosis
due to other causes.
. They result from a combination ofpapillary necrosis and parenchymal destruction. Typically,the papillae are involved first and this is followed by corticaldamage. Communication with the collecting system resultsin thickening, ulceration, and fibrosis – often with strictureformation
Treatment begins with an intensive phase of 2 monthsof daily INH, rifampin, and pyrazinamide, followed by a continuation phase of 4 months of INH and rifampin given daily, or alternatively thrice weekly
Although 6 months is the duration of standard short-coursetherapy, clinical scenarios regularly arise that require prolongationof treatment. Both the type of clinical disease present and the antituberculous drugs used affect duration of treatment
Monitor liver enzymes foer hepatic toxicity
Abstaind form alcohol and hepatotoxic drugs
Close follow uop recommended because to monitor side effects and renal lesion may worsen during treatment
Healing is accompanied by new fibrosis which cause urinary obstruction and bladder contraction
Steroids may help in the managent
Optimal timing of surgery is 4-6 weeks after initiation of medical therapy
Inflammation to subside
Bacillary load to decrease
Lesions to stabilize
A tuberculous cutaneous fistula can develop if the PCN is simply removed, although this is less likely to develop with effectiveconcurrent medical therapy.
High contrast injection pressures should be avoided during stent or PCN to prevent possible dessimintation of infection
total nephrectomy is considered in
two settings.
The first is the patient with a nonfunctional kidney and
recalcitrant or recurrent TB despite optimal medical therapy.
After
nephrectomy of the infected kidney, relapse rates of less than 1%
have been reported after short-course medical treatment (Figueiredo
and Lucon, 2008). The second setting in which a nephrectomy is
considered is the patient with a nonfunctional kidney and medically
resistant hypertension. Nephrectomy improves hypertension in 65% o
The length and degree ofthe stricture, whether it can be passed by a guidewire or not, vascularsupply to the lesion, and renal function are important factors to beconsidered in the management of patients
. In general, short strictures
with residual lumens in patients with good renal function yield
the best outcome. Strictures forming during medical treatment and
managed by early stenting (double-J placement) can stabilize and
require no further treatment (
Upper and middle ureteric strictures can be managed by excision
of the diseased segment, and, with adequate mobilization, a primary
tension-free ureteroureterostomy can be performed. Alternatively,
lysis of adhesions and intubation (Davis intubated ureterotomy) may
be done. Lower ureter strictures requiring surgery are best managed
by complete excision of the entire affected ureteric segment back to
healthy ureteric mucosa that has good blood supply. The resultant
gap is bridged with a tension-free, well-vascularized anastomosis to
healthy bladder (ureteroneocystostomy). Various procedures exist to
bring the bladder closer to the ureteric end. Simple mobilization
of the lateral attachments of the bladder on the contralateral side,
accompanied by dividing the superior vesical artery, may provide
2 to 3 cm of length to bridge a small gap. In patients with good
bladder capacity, a psoas hitch may also be performed. Care must be
taken to avoid the genitofemoral and femoral nerves when placing
these sutures. A well-performed psoas hitch can bridge a gap of up
to 5 cm. A Boari flap is another method of bridging a longer gap of
10 to 15 cm and may be performed in combination with a psoas
hitch (Sankari, 2007). A poorly executed Boari flap can compromise
bladder capacity. Contracted bladders from TB cystitis may not have
sufficient surface area and elasticity to allow flap creation. Finally,
ileal interposition (ileal ureteric replacement) can be done in cases
of multiple or recurrent strictures in which the native ureter is no
2.Thimble bladder with <20ml capacity best managed by
orthotopic bladder substation
Complication-
mucus production
Electrolyte derangements and
secondary bacterial infection