Lesson 2

Lesso2                                  

ACUTE nPYELONEPHRITIS

 

Etiology

Acute npyelonephritis is an infectious inflamma­tory disease that involves both the nparenchyma and the pelvis of the kidney; it may affect one or, on occasion, nboth kidneys.

Aerobic ngram-negative bacteria are the principal causative agents; common strains of E ncoli are the predominant pathogens. All species of Proteus are nespecially important because they are potent producers of urease, an enzyme nthat splits urea and produces highly alkaline urine that favors the nprecipitation of phosphates to form magnesium ammonium phosphate (struvite) and ncalcium phosphate (apatite) stones. Klebsiella species are less potent nproducers of urease but elaborate other substances that favor urinary stone nformation.

Gram-positive nbacteria other than the enterococ-cus Streptococcus faecalis seldom ncause pyelone­phritis. Staphylococci may infect the kidney by the hematogenous nroute and cause bacteriuria and renal abscesses. Obligate anaerobic bacteria nrarely cause pyelonephritis.

 

Pathogenesis n

Renal ninfection usually ascends from the urethra and lower genitourinary tract. nHematogenous infec­tion of the kidney occurs infrequently; lymphatic spread noccurs rarely, if ever.   

                                     

 

n

Microbial      organism	Acute uncomplicated cystitis (%)*	Acute uncomplicated pyelonephritis (%)	Complicated UTI(%)	Catheter-associated UTI (%)
Escherichia coli	68	89	32	24
Staphylococcus saprophyticus	8	0	1	0
Proteus	6	4	4	6
Klebsiella	4	4	5	8
Enterococci	3	0	22	7
Pseudomonas	0	0	20	9
Mixed	3	5	10	11
Yeast	0	0	15	8

 

 

 

The nshort urethra in girls and women and its close proximity to the anus allow nperiurethral pathogenic bacteria easy access to the bladder during sexual inter­course nor urethral manipulation. Girls and women with breached local defenses due to nbiologic, anatomic, or other abnormalities frequently experience introital and nperiurethral colonization by pathogenic enteric bac­teria and are especially nprone to infection that ascends from the urethra.

Males nare less susceptible to ascending urethral infection because the male urethra nis much longer than the female urethra and the meatus is not so near the anus nand because the prostate normally secretes an­tibacterial factors that give nsome protection against invading pathogens.

Once npathogenic bacteria reach the bladder via the urethra, whether infectiobecomes established is influenced by the quality of the bladder defenses: the nefficacy of voiding and muscle coordination, the anti­microbial properties of nthe urine, and factors that allow or inhibit bacterial adherence to surface ncells.

Once nbladder infection is established, whether infection ascends via the ureters and ninvolves the kid­neys is influenced by microbial virulence factors, the npresence or absence of vesicoureteral reflux, the qual­ity of ureteral nperistalsis, and the susceptibility of the renal medulla to infection.

 

 

    Infectiogoes at the ureter from the bladder because of the        vesicoureteral reflux.

 

 

 

                        The secondary npyelonephritis goes with urostasis

 

 

 

 

 

Causes

Common causes

Ascending UTI: 75% of npyelonephritis cases are due to E. coli; 10% to 15% are caused by other nGram-negative rods, Klebsiella, Proteus, Enterobacter; others include nPseudomonas, Serratia, and Citrobacter. Gram-positive agents include nEnterococcus faecalis and, less commonly, Staphylococcus aureus anaerobes

Fungal agents, especially nCandida spp., are seen in immunocompromised patients and patients with diabetes

Rare causes

Other infecting organisms may ninclude Salmonella, Leptospira, Mycoplasma, Chlamydia

In travelers, the possibility nof tropical infection and Echinococcus should be kept in mind

Contributory or predisposing nfactors

Diseases or conditions that ncause stasis of urine in the urinary tract promote multiplication of organisms nin the urinary tract and ascension of infection

Diseases that impair immunity promote nmultiplication of organisms in the urinary tract and ascension of infection

Presence of a device in the nurinary tract promotes multiplication of organisms in the urinary tract and nascension of infection

 

Obstructions to urine flow:

Vesicoureteric reflux (VUR) is nthe most important predisposing factor in children younger than 6 years

Obstruction of outflow of nbladder: benign prostatic hypertrophy, prostatic carcinoma, bladder tumors

Carcinoma arising from renal ntract, for example, renal cell carcinoma, bladder cancer, ureteric tumors; ncarcinoma arising outside renal tract and impinging on it, for example, bowel, ncervix, prostate

Radiotherapy or surgical ndamage to ureters

Pregnancy encourages reflux by ndilatation of the ureters and probably reduces immunity of renal parenchyma

Calculi cause obstruction and nstasis, and act as foci for infection

Neurologic abnormalities, for nexample, spina bifida, multiple sclerosis

Polycystic kidney disease, naffects 0.8/1000 of the population and is inherited as an autosomal dominant ntrait

Renal parenchymal damage due nto tuberculosis

Neurogenic bladder following ntrauma or secondary to neurologic disorders such as diabetic neuropathy

 

Impaired immunity:

HIV

Myeloproliferative disorders

Diabetes

Organ transplantation (transplant npyelonephritis of the new kidney)

Chemotherapy

Stasis and impaired immunity nmay coexist in patients with:

Malignancy, especially after nchemotherapy

Diabetes

Devices in the urinary tract:

Indwelling bladder catheters n(Foley catheters)

Ureteral stents

 

Classification

    nThe primary and secondary pyelonephritis are ndistinguished.

    nThere is  no ndysfunction of the  urine  outflow during the primary pyelonephritis.

    nThe secondary pyelonephritis goes with urostasis.

 

    n1/ The unilateral and bilateral.

    n a/ Acute /purulent, nserous/

    n b/ Chronic;

    n c/ Relapsing ncourse.

    n2/ By the mode of bacteria pathway there are ndiffered                             

    n3/ a/ hematogenous /ascending/;

    nb/ urogenic /ascending/;

    nc/ urolithiasis /infected urinary stones/;

    nd/ tuberculosis of the kidneys;                                                                   n

    ne/ the other renal diseases.

    nBy the course, age, stage of the organism there are ndiffered:

    n1/ the pyelonephritis of newborn;

    n2/ the pyelonephritis of the aged patients;

    n3/ the pyelonephritis of the pregnant women;

    n4/ the pyelonephritis in diabetes mellitus patients.

    nThe acute pyelonephritis may be complicated with npurulent nephritis, carbuncle of the kidney, the renal abscess, renal ninsufficiency.

 

 

Clinical nFindings

A. Symptoms Symptoms

Back pain orflank pain

Chills with shaking

Severe abdominal pain (occurs occasionally)

Fatigue

Fever

Higher than 102 degrees Fahrenheit

Persists for more than 2 days

General ill feeling

Chills with shaking

Mental changes or confusion*

 Skin changes

Flushed or reddened skin

Moist skin (diaphoresis)

Warm skin

 Urinatioproblems

Blood in the urine

Cloudy or abnormal urine color

Foul or strong urine odor

Increased urinary frequency or urgency

Need to urinate at night (nocturia)

Painful urination

Vomiting, nausea

 

    nMental changes nor confusion may be the only signs of a urinary tract infection in the elderly

 

 

B. Signs: nThe classic presentation in patients with acute pyelonephritis is as follows:

 

Fever – nThis is not always present, but when it is, it is not unusual for the ntemperature to exceed 103°F n(39.4°C)

 

Costovertebral nangle pain – Pain may be mild, moderate, or severe; flank or costovertebral nangle tenderness is most commonly unilateral over the involved kidney, although nbilateral discomfort may be present

 

Nausea nand/or vomiting – These vary in frequency and intensity, from absent to severe; nanorexia is common in patients with acute pyelonephritis

 

Gross nhematuria (hemorrhagic cystitis), unusual in males with pyelonephritis, occurs nin 30-40% of females, most often young women, with the disorder.

 

Symptoms nof acute pyelonephritis usually develop over hours or over the course of a day nbut may not occur at the same time. If the patient is male, elderly, or a child nor has had symptoms for more than 7 days, the infection should be considered ncomplicated until proven otherwise.

 

The nclassic manifestations of acute pyelonephritis observed in adults are ofteabsent in children, particularly neonates and infants. In children aged 2 years nor younger, the most common signs and symptoms of urinary tract infection (UTI) nare as follows:

 

Failure nto thrive

 

Feeding ndifficulty

 

Fever

 

Vomiting

 

Elderly patients may present with typical nmanifestations of pyelonephritis, or they may experience the following:

 

Fever

 

Mental nstatus change

 

Decompensatioin another organ system

 

Generalized ndeterioration

 

 

C. Laboratory nFindings: The hemogram typi­cally shows significant leukocytosis n(polymorphonu-clear neutrophils and band cells); the erythrocyte sedimentatiorate is increased. Urinalysis usually shows cloudy fluid with heavy pyuria, nbacteriuria, mild proteinuria, and often microscopic or gross hematuria. nLeukocyte casts and glitter cells (large polymorphonuclear neutrophils ncontaining cytoplas-mic particles that exhibit dramatic brownian move­ment) are noccasionally seen. Quantitative urine culture generally grows the responsible npathogen in heavy density (≥100,000 colonies/mL); sensitivity tests are nhelpful in therapy and of vital importance in the man­agement of complicating nbacteremia. Serial blood cul­tures are indicated, because bacteremia commonly nac­companies acute pyelonephritis. In uncomplicated acute pyelonephritis, total nrenal function generally re­mains normal, and the serum creatinine level is not nelevated.

 

 

Diagnosis

 

In the noutpatient setting, pyelonephritis is usually suggested by a patient’s history nand physical examination and supported by urinalysis results. Urine specimens ncan be collected through the following methods:

 

Cleacatch

Urethral ncatheterization

Suprapubic nneedle aspiration

Urinalysis ncan include the following:

Dipstick nleukocyte esterase test (LET) – Helps to screen for pyuria

Nitrite nproduction test (NPT) – To screen for bacteriuria

Examinatiofor hematuria (gross and microscopic) and proteinuria

 

Urine nculture is indicated in any patient with pyelonephritis, whether treated in ainpatient or outpatient setting, because of the possibility of antibiotic nresistance.

 

Imaging nstudies that may be used in assessing acute pyelonephritis include the nfollowing:

 

Computed ntomography (CT) scanning – To identify alterations in renal parenchymal nperfusion; alterations in contrast excretion, perinephric fluid, and nonrenal ndisease; gas-forming infections; hemorrhage; inflammatory masses; and nobstruction

 

Magnetic nresonance imaging (MRI) – To detect renal infection or masses and urinary nobstruction, as well as to evaluate renal vasculature

 

Ultrasonography n- To screen for urinary obstruction in children admitted for febrile illnesses nand to examine patients for renal abscesses, acute focal bacterial nephritis, nand stones (in xanthogranulomatous pyelonephritis)

 

Scintigraphy n- To detect focal renal abnormalities

 

CT and nMR urography – Used in the evaluation of hematuria

 

X-Ray nFindings:

 

                  Plain film

 

 A plain film of nthe abdomen may show some degree of obliteration of the renal outline owing to nedema of the kidney and perinephric fat. Suspicious calcifications, must be ncarefully evaluated, because infected renal stones and calculous obstructiocomplicating pyelonephritis require spe­cial management.

           Excretory urograms

 

Excretory nurograms performed during the acute stage of uncomplicated pyelonephritis nusually show few abnormalities but are important in surveying for possible ncomplicating factors. The severely infected kidney may appear enlarged, show a ndecreased nephrogram effect on the initial film, and reveal little or no ncaliceal radiopaque material. Following appropriate therapy, the urograms nreturn to normal.

Voiding cystograms are best delayed until several weeks after the ninfection is cleared; otherwise, tran­sient vesicoureteral reflux, ofteassociated with the accompanying cystitis, may be confused with more serious npermanent reflux.

 

Retrograde cystogram n(vesicoureteral reflux)

E. nRadionuclide Imaging: At times, imaging ‘ the kidneys with ngallium-67 helps to determine the site of infection and distinguish betweeacute pyelone­phritis and renal abscess. Despite some false-positive and nfalse-negative images, Hurwitz et al (1976) claim 86% accuracy in confirming nacute pyelonephritis by this method.

 

Instrumental Examination

 

                 

 

    nThere can be seen the nbullous edema of the urethral orifice because of calculus at the intravesical nportion, ureterocele, tumor compression.

    Chromocystoscopia shows the range even sometimes the cause of the nfunctional loss of the urine outflow.

 

 

                                                                                           nDifferential Diagnosis

Differential nDiagnosis

Because nof the location and nature of the pain, pancreatitis at times may be confused nwith acute py­elonephritis. Elevated serum amylase and normal re­sults of nurinalysis help to confirm a diagnosis of pan­creatitis and rule out npyelonephritis.

Basal npneumonia is a febrile illness that causes pain in the subcostal area. The npleuritic nature of the pain and the chest x-ray usually allow differentiation.

Acute nintraabdominal disease, including such conditions as acute appendicitis, ncholecystitis, and di-verticulitis, must at times be distinguished from acute npyelonephritis. Although the signs and symptoms may be confusing initially, the nnormal urinalysis associated with primary gastrointestinal disease and other laboratory ntests should make the differential diagnosis un­complicated.

Iwomen, the onset of acute pelvic inflammatory disease (PID) at times must be ndistinguished from acute pyelonephritis. Characteristic physical findings and nnegative urine cultures should make differentia­tion fairly easy.

In male npatients with febrile genitourinary tract infection, the main differential ndiagnosis consists of acute pyelonephritis, acute prostatitis, and acute nepididymoorchitis. Characteristic physical findings and symptoms in prostatitis nand epididymitis should make this differentiation easy.

Acute npyelonephritis must be distinguished from renal abscess and perinephric nabscess. Radiographic studies often are necessary to confirm the specific ndiagnosis.

Treatment                                                                                                      

 

Ambulatory younger women who present with signs and nsymptoms of uncomplicated acute pyelonephritis may be candidates for outpatient ntherapy. They must be otherwise healthy and must not be pregnant. In addition, nthey must be treated initially in the emergency department (ED) with vigorous noral or IV fluids, antipyretic pain medication, and a dose of parenteral nantibiotics. Studies have shown that outpatient therapy for selected patients nis as safe as inpatient therapy for a comparable group of patients and is much nless expensive.

Use analgesics as needed. Early in the course of the nillness, parenteral analgesics are ofteecessary to reduce morbidity from nsymptoms. Nonsteroidal anti-inflammatory drugs and narcotics are complementary; ndo not assume that one class is better than the other.

Admission is usually appropriate for patients who nare severely ill, pregnant, or elderly or who have comorbid disorders that nincrease the complexity of management or the complication rate (eg, diabetes nmellitus, chronic lung disease, congenital or acquired immunodeficiency). nAdmission may also be advisable for patients whose social situation is nunstable, because of the possibility of poor compliance or poor follow-up.

Emergency surgery may be indicated in a patient with nfever or positive blood culture results persisting longer than 48 hours; in a npatient whose condition deteriorates; or in a patient who appears toxic for nlonger than 72 hours. These patients may have an abscess, emphysematous npyelonephritis, or an obstructing calculus. The etiology may not be immediately nevident, but an unexpected change in the clinical picture warrants immediate nevaluation for potential surgical intervention.

After recovery from the acute infection, patients nmay be candidates for elective surgery to reverse conditions that predispose nthe kidney to recurrent infections and renal damage. These conditions include ncongenital anomalies, fistulae involving the urogenital tract, prostatic nhypertrophy, renal calculi, and vesicoureteral reflux.

 

 

 

 

 

 

A. Specific nMeasures: When the infection is se­vere or complicating factors are npresent, hospitalization may be required. Urine and blood specimens must be nobtained immediately for culture; recognized pathogens must be tested for nantimicrobial sensitivity. Until the results of these tests are known, nantimicrobial drugs should be given empirically. Although clinicians differ itheir choice of antimicrobial agents, our pref­erence is to administer aaminoglycoside (amikacin, gentamicin, or tobramycin) plus ampicillin intrave­nously nin full dosage. If the pathogen is sensitive and the clinical response is nfavorable, this treatment is continued for about 1 week and then re­placed with nan appropriate oral antimicrobial drug for an additional 2 weeks. Complicating nfactors, eg, obstructive uropathy or infected stones, must be rec­ognized early nand dealt with effectively if complica­tions are to be avoided.

B. General nMeasures: Complete bed rest is ad­vised until symptoms subside. Medicatioshould be given for pain, fever, and nausea. It is important to give fluids nintravenously and orally to ensure adequate hydration and maintenance of nadequate urinary output.

C. Failure nof Response: If the clinical response remains poor after 48-72 hours of ntherapy, reevalua-tion is necessary to assess for possible complicating factors n(eg, obstructive uropathy) or the use of inap­propriate drugs. Excretory urography nis required; if this is contraindicated, retrograde urography must be done. nUnless treated quickly and effectively, obstruc­tive uropathy complicating nacute pyelonephritis can lead to bacteremia and irreversible renal damage.

 

 

              Ureteral ncatheterization

 

 

 

 

  PERCUTANEOUS NEPHROSTOMY

 

 

 

Antimicrobial nAgents Used in the Treatment of Acute Pyelonephritis

 

 

n

Agent	Dosing schedule	Oral dose	IV dose	Comments
Amoxicillin	Every 8 to 12 hours	500	–	None
Amoxicillin- clavulanate potassium (Augmentin)	Every 8 to 12 hours	500/125	–	GI side effects*
Ampicillin-sulbactam (Unasyn)	Every 4 to 6 hours	–	150 to 200 mg per kg per day	GI side effects*
Aztreonam (Azactam)	Every 6 to 8 hours	–	1 to 2 g	Phlebitis; GI side effects*
Cefotaxime (Claforan)	Every 8 to 12 hours	–	1 to 2 g	Thrombophlebitis
Ceftriaxone (Rocephin)	Once in 24 hours	–	1 to 2 g	Leukopenia; elevated BUN
Cephalexi (Keflex)	Every 6 hours	500	–	GI side effects*
Ciprofloxaci (Cipro)	Every 12 hours	500	400 mg	Nausea; headache; photosensitivity; pregnancy category C
Norfloxacini	Every 12 hours	500	400 mg	Nausea; headache; photosensitivity; pregnancy category C

 

 

 

Regimens nfor complicated cases

 

With complicated acute pyelonephritis, treat npatients parenterally until defervescence and improvement in the clinical ncondition warrants changing to oral antibiotics. Complete the course of therapy nwith an oral agent selected on the basis of culture results.Acceptable regimens ninclude the following:

 

Ampicillin and an aminoglycoside

 

Cefepime

 

Imipenem

 

Meropenem

 

Piperacillin-tazobactam

 

Ticarcillin-clavulanate

 

If the patient is allergic to penicillin, it should nbe substituted with vancomycin. Vancomycin or linezolid are options if enterococci nare a consideration.

 

 

 

 

D. Follow-Up nCare: Clinical improvement does not always nimply cure of the infection. In about one-third of patients, symptoms improve ndespite persis­tence of the bacterial pathogen. Therefore, repeat urine ncultures are important during and after therapy for a follow-up period of at nleast 6 months.

 

Prognosis

Wheidentified promptly and treated appropri­ately in a patient who has no nunderlying complicating factors, acute pyelonephritis carries a good prognosis nfor cure without sequels. The likelihood of serious sequels and a less nfavorable prognosis varies with the severity of complicating factors and the npatient’s age at the onset.

 

Possible Complications

Acute nkidney failure

Kidney ninfection returns

Infectioaround the kidney (perinephric abscess)

Severe nblood infection (sepsis)

 

Prevention

 

Prompt nand complete treatment of bladder infections may prevent development of many ncases of pyelonephritis. Chronic or recurrent urinary tract infection should be ntreated thoroughly.

 

You cahelp preventing kidney infections by taking the following steps:

Keep nthe genital area clean. Wiping from front to back helps reduce the chance of nintroducing bacteria from the rectal area to the urethra.

Urinating nimmediately after sexual intercourse. This may help eliminate any bacteria that nmay have been introduced during sexual activity.

Drink nmore fluids (64 to 128ounces per day). This encourages frequent urination and nflushes bacteria from the bladder.

Drink ncranberry juice. Doing so prevents certain types of bacteria from attaching to nthe wall of the bladder and may lessen your chance of infection.

 

 

 

 

 

 

 

 

Gestation pyelonephritis.

(Pyelonephritis of pregnancy).

                   

 

Acute npyelonephritis is a bacterial infection of the kidneys, which affects 1 to 2% nof pregnant women. In most cases, the infection first develops in the lower nurinary tract. If not diagnosed and treated properly, the infection may ascend nfrom the urethra and genital area to the bladder, then to one or both kidneys.

 

Compared to nnon-pregnant women, pregnant women are more likely to develop pyelonephritis. nThis is due to physiological changes during pregnancy that can interfere with nthe flow of urine. Normally, the ureters drain urine from the kidney into the nbladder and out of the body through the urethra. But, during pregnancy, the nhigh concentration of the hormone progesterone can inhibit contraction of these ndrainage ducts. Also, as the uterus becomes enlarged during pregnancy, it can compress nthe ureters. These changes can lead to problems with proper drainage of the nurine from the kidneys, causing the urine to remain stagnant. As a result, nbacteria in the bladder, rather than being washed out of the system, may nmigrate to the kidneys and cause infection. The Escherichia coli (E. Coli) nbacterium is the usual culprit. Other bacteria-such as Klebsiella pneumoniae, nProteus species, and staphylococci-can also cause kidney infections. About 75 nto 80% of cases of pyelonephritis occur on the right side, 10 to 15% are nleft-sided, and about 10% are bilateral.

Pyelonephritis is nan infection of the uppermost section of the urinary tract. The condition is nmore common in women with asymptomatic urinary tract or bladder infection. nStudies have identified a risk ratio of 14 to 1,000. This means about 14 cases nof acute pyelonephritis are diagnosed per 1,000 pregnancies. It is estimated nthat up to 70-percent of cases can be avoided with regular urine cultures and nsubsequent treatment for bacterium present in urine. Treatment for urinary ninfections, including bladder infections and pyelonephritis, is a course of nantibiotics.

 

Causes of Pyelonephritis

Pyelonephritis noccurs more frequently in pregnant patients due to increased progesterone and npressure placed on the ureters by the growing uterus. In about 85-percent of ncases, E. coli is the bacterium responsible for infection though other nbacterium, including staphylococcus and group D streptococci may also be nresponsible.

 

The inflammatory nprocess develops while pregnancy, delivery and puerperal period. Most nfrequently it is observed in pregnant (48%) more rare in puerperal (35%) women. nIt develops while 1 pregnancy 2 trimester often. There are women 18-25 years nold. That is explained by a not complete adaptation to immunologic, hormone nchanges of the pregnancy. It is supposed not to be a primary disease but nactivation of latent pyelonephritis.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Urinoculture finds nout E.Coli, Staphylococcus albicans, Clebsiella in pregnant women. Associatioof the Proteus and Blue pus bacilli is observed in puerperal women. The primary nsource of the infection may be any purulent inflammatory place (furunculosis, ndental caries, inflammatory diseases of the genital organs).

The pathogenetic nsign is bacteriuria. It is observed in 7% only. Urodynamic dysfunction favors nthe pyelonephritis development. Pathogenesis may be explained with mechanical, nneurohumoral and endocrine factors. The enlarged uterus compresses the pelvic nportion of the ureters causing ureteropyeloectasia while pregnancy. Urostasis nat the upper portion develops because of decreasing of the ureteral muscles and npelvises of the kidney tension.

The moderate nhypotonia and hypokinesia of the calicopelvic of the both kidneys and ureters nare observed on 8^th week.

Changes of the nupper portion of the urinary tract may be explained by weakening of the nsympathetic nervous system tonus. Dysfunction of the urinary output because of nthe urinary pathway atonia is a condition for pathogen activation. nVesicoureteral and pelvicorenal refluxes favor spreading of the infection into nthe interstitial tissue of the renal parenchyma (medulla of the kidney).

Acute npyelonephritis of pregnancy. Primary acute process acute rarely. This is an active nphase of the chronic process frequently. The prepueral women have attacks of nthe acute pyelonephritis at the 4-, 6-, 12- day of the puerperal period (these nare days of the postpartum complications: endometritis, metrophlebitis).

Urinary tract ninfection

 

UTI is defined as nthe presence of at least 100,000 organisms per milliliter of urine in aasymptomatic patient, or as more than 100 organisms/mL of urine with naccompanying pyuria (> 7 white blood cells [WBCs]/mL) in a symptomatic npatient. A diagnosis of UTI should be supported by a positive culture for a nuropathogen, particularly in patients with vague symptoms. UTIs are associated nwith risks to both the fetus and the mother, including pyelonephritis, preterm nbirth, low birth weight, and increased perinatal mortality.

 

Asymptomatic bacteriuria

Asymptomatic nbacteriuria is commonly defined as the presence of more than 100,000 norganisms/mL in 2 consecutive urine samples in the absence of declared nsymptoms. Untreated asymptomatic bacteriuria is a risk factor for acute ncystitis (40%) and pyelonephritis (25-30%) in pregnancy. These cases account nfor 70% of all cases of symptomatic UTI among unscreened pregnant women.

 

Acute cystitis

Acute cystitis ninvolves only the lower urinary tract; it is characterized by inflammation of nthe bladder as a result of bacterial or nonbacterial causes (eg, radiation or nviral infection). Acute cystitis develops in approximately 1% of pregnant npatients, of whom 60% have a negative result on initial screening. Signs and nsymptoms include hematuria, dysuria, suprapubic discomfort, frequency, urgency, nand nocturia. These symptoms are often difficult to distinguish from those due nto pregnancy itself.

 

Acute cystitis is ncomplicated by upper urinary tract disease (ie, pyelonephritis) in 15-50% of ncases.

 

Acute pyelonephritis

Pyelonephritis is nthe most common urinary tract complication in pregnant women, occurring iapproximately 2% of all pregnancies. Acute pyelonephritis is characterized by nfever, flank pain, and tenderness in addition to significant bacteriuria. Other nsymptoms may include nausea, vomiting, frequency, urgency, and dysuria. nFurthermore, women with additional risk factors (eg, immunosuppression, ndiabetes, sickle cell anemia, neurogenic bladder, recurrent or persistent UTIs nbefore pregnancy) are at an increased risk for a complicated UTI.

Risks of Other Pregnancy Complications Associated with nPyelonephritis

 

Untreated npyelonephritis may cause other pregnancy complications, including respiratory ndistress, anemia and impaired kidney function. About 20-percent of severe cases nlead to septic shock with acute respiratory and kidney malfunction. About n5-percent of women with an acute form of the infection will suffer preterm ndelivery

 

 

 

Clinical findings.

Clinical findings nhave the own peculiarities according to the different terms of pregnancy. They nalso depend on the range of the urinary output damage. A sharp pain in loithat irradiates to the lower portions of the abdomen, genitals are at the 1 ntrimester. 2^nd and 3^rd trimesters are characterized with na moderate pain because of the dilatation of the upper urinary tract and nintrarenal pressure decreasing.

An acute purulent npyelonephritis develops more frequently in pregnant and postpueral women. There nis a high lethality rate caused by an acute purulent pyelonephritis.

 

Diagnosis is rather difficult. The enlarged uterine nhinders the palpation. The right kidney damage should be differed from the nacute appendicitis and cholecystitis.

 

 

 Ultrasonography n(shows dilatation of the calyces and renal pelvis, dysfunction of the urine npassages, edema of the adipose capsule looks as rarefaction about the kidney)

 

 

 Ultrasonography

 

 

 

 

 

X-ray imaging is ninadmissible exclusive rare occasions.

 

          Chromocystoscopia

 

The endoscopy ninvestigation isn’t recommended too. In case of the suspicion of purulent nprocess the complete clinical research is required including Chromocystoscopia, nradionuclide renography, scanning, excretory urography, ultrasonography. The ndelayed excretion of the indigocarmine while Chromocystoscopia is attended to npeculiar urodynamic due to pregnant uterus.

 

 

Treatment.                                                                                

Caesar’s incisioby retroperitoneal access is performed because of an acute inflammation at the nlast days of pregnancy.

Antibiotics nshouldn’t be harmful to fetus. The natural and semisynthetic penicillines are nrecommended at the 1^st trimester. Wider choice of antibiotics is at nthe 2^nd and 3^rd trimesters because placenta has its nbarrier function then.

The puerperal womemay transfer drugs to child with milk.

Treatment should be ncontinuous. Nitrofuranes are admissible after 2^nd month in dosage n50-100mg per day. Nalidixone acid is admissible after the 4^th month nof pregnancy (2g per day for 2-3 weeks). But its administration must be stopped nbefore delivery.

 

 

Table. Treatment of Pyelonephritis During nPregnancyMild to moderate pyelonephritis

 

ceftriaxone n(Rocephin) 1 g nIV q24h or

 

cefepime (Maxipime) n1 g IV nq12h or

 

cefotaxime n(Claforan) 1-2 g nIV q8h or

 

ceftazidime n(Fortaz, Tazicef) 2 g nIV q8h or

 

ampicillin 1-2 g IV q6h plus gentamicin IV n1.5 mg/kg q8h

Severe pyelonephritis

If patient is nimmunocompromised and/or has incomplete urinary drainage:

 

ticarcillin-clavulanate n(Timentin) 3.1 g nIV q6h or

 

ampicillin-sulbactam n(Unasyn) 1.5 g nIV q6h or

 

piperacillin-tazobactam n(Zosyn) 3.375 g nIV q6h

 

 

 

 

 

 

 

 

  Ureteral catheterization

 

 

The acute purulent npyelonephritis in pregnant women requires the obligate surgical measures. Its nscope depends on form of the disease. It is necessary anyway until the ndelivery.

Approximately 20 to 30% of pregnant patients with npyelonephritis develop recurrent infections later in pregnancy. The most ncost-effective way to lower your risk of recurrence is to take a single dose of nan antibiotic daily, as a preventive measure. Sulfisoxazole (Gantrisin), 1g, or nnitrofurantoin monohydrate macrocrystals (Macrobid), 100 mg, are appropriate noptions.

 

Prognosis

In most cases of bacteriuria and urinary tract ninfection (UTI) in pregnancy, the prognosis is excellent. The majority of nlong-term sequelae are due to complications associated with septic shock, nrespiratory failure, and hypotensive hypoxia (ie, extremity gangrene).

 

Maternal UTI has few direct fetal sequelae because nfetal bloodstream infection is rare; however, uterine hypoperfusion due to nmaternal dehydration, maternal anemia, and direct bacterial endotoxin damage to nthe placental vasculature may cause fetal cerebral hypoperfusion.

Untreated upper UTIs are associated with low birth nweight, prematurity, premature labor, hypertension, preeclampsia, maternal nanemia, and amnionitis. A retrospective population-based study by Mazor-Dray et nal showed that UTI during pregnancy is independently associated with nintrauterine growth restriction, preeclampsia, preterm delivery, and cesareadelivery.

 

 

 

 

RENAL ABSCESS (Renal Carbuncle)

 

 

 

 

                                  

An abscess is a localized collection of pus in a nhollow area formed by the breaking up of tissues. A renal abscess is one that nis confined to the kidney and is caused either by bacteria from an infectiotraveling to the kidneys through the bloodstream or by a urinary tract infectiotraveling to the kidney and then spreading to the kidney tissue.

A renal abscess is a very unusual disease, but ngenerally occurs as a result of common problems such as kidney inflammation, nstone disease and vesicoureteral reflux. Occasionally, a renal abscess cadevelop from a source of infection in any area of the body. Multiple skiabscesses and intravenous drug abuse can also be sources of renal abscess. nComplicated urinary tract infections associated with stones, pregnancy, nneurogenic bladder and diabetes mellitus also put a person at risk for renal nabscess.

 

 

Etiology

Renal ncortical abscesses develop primarily as a result of hematogenous spread of Staphylococcus naureus infections at distant sites (most often the skin). At times, foci of nprimary renal infections caused mainly by gram-negative bacteria (coliform norganisms) coalesce in the renal medulla to form abscesses. In the past, most nrenal abscesses were caused by staphylococci; recently, coliform bacteria have nbecome the predominant pathogens in renal abscesses. Renal abscesses caused by nobligate anaerobic bacteria are rare.

 

 

 

 

        Pathogenesis & Pathology 

                               

 

Aabscess (carbuncle) caused by S aureus de­velops from hematogenous spread nof the organism from a primary skin lesion. Intravenous drug abusers are nespecially prone to develop staphylococcal renal abscesses. Multiple focal nabscesses evolve and even­tually coalesce to form a multilocular abscess. Un­treated ncortical abscesses may rupture into the pyelocaliceal system or into the nperinephric space (perinephric abscess). Urinary tract infection occurs only if nthe abscess communicates with the pyelocaliceal sys­tem.

The nmore common type, renal medullary abscess, evolves from acute or chronic foci nof pyelonephritis, often associated with ureteral obstruction or calculous ndisease (calculous pyonephrosis). The infecting pathogens usually are ngram-negative rods. Timmons and Perlmutter (1976) believe that gram-negative nbacillary abscesses in children may be a complication of vesicoureteral reflux, nwith the pathogens invading the collecting tubules. In adults, the kidney nusually is damaged by chronic suppurative pyelonephritis that may culminate ione or more abscesses. Medullary abscesses may also rupture into the nperinephric space. One-third of affected patients are diabetics.

 

 

Clinical nFindings

A. Symptoms: Staphylococcal renal nabscess is typified by an abrupt onset of chills, fever, and lo­calized ncostovertebral pain. In the early stages, when the abscess does not communicate nwith the collecting system, symptoms of vesical irritability are absent and nurinalysis is normal, although the patient may appear quite septic. The nclinical picture often mimics that of acute pyelonephritis.

In most npatients with medullary abscesses due to gram-negative rods, there is a history nof persistent or recurrent bouts of urinary tract infection, often as­sociated nwith urolithiasis, obstructive uropathy, or renal surgery.

B. Signs: nIn acute cases, localizing signs are flank tenderness, possibly a palpable nmass, and erythema and edema of the skin of the overlying loin. At times, nhowever, abscesses associated with both acute and chronic infections present as nfebrile illnesses with few localizing signs.

C. Laboratory nFindings: The hemogram usu­ally shows marked leukocytosis with a shift to nthe left. With cortical abscesses that do not communicate with the collecting nsystem, urinalysis shows no pyuria or bacteriuria, and urine culture is nnegative. Medullary abscesses generally are associated with heavy pyuria, nbacteriuria, and positive urine cultures. The sudden appearance of heavy pyuria nand bacteriuria may herald the rupture of a previously noncommunicating abscess ninto the collecting system. Blood cultures may be positive.

Depending nupon the extent of renal involvement and associated renal abnormalities, the nserum creatinine and urea nitrogen values may be normal or elevated. Since npatients with renal abscesses often are diabetic, glycosuria and hyperglycemia nmay be found.

D. X-Ray nFindings: If the renal outline is visi­ble, the plain film may show aenlarged kidney or a bulge of the external renal contour. With perinephric nedema, however, often the renal outline is obliterated and the psoas shadow nindistinct. Unless the abscess has ruptured into the perinephric space or is nquite large, scoliosis generally is not observed. Renal stones may be noted. nWhen cortical abscesses are small, the excretory urogram may appear normal; nmost often, however, a space-occupying lesion (the abscess) is delineated. nPyelonephritic changes, hydronephrosis, and urolithiasis also may be observed. nDelayed opacification or even a nonfunctioning kidney may be found.

   Excretory nurogram

 

 

 

 

 

 

                          KUB n   

      Excretory nurogram

 

Renal nangiography usually makes the diagnosis. The abscess fails to opacify; its nwalls are irregular. Surrounding vessels are displaced, and hypervascularity is ncommon. The most important sign is excessive capsular vessels overlying the nabscess.

 

E. Ultrasonography:

 

 Ultrasonography

 

 Renal echograms ngener­ally distinguish simple cysts (no internal echoes) from solid masses n(many internal echoes) but often fail to distinguish renal abscesses from nmalignant lesions, particularly necrotic, cystic renal cell carcinomas. nPercutaneous needle aspiration of the mass under ul­trasonic guidance may nconfirm the diagnosis.

 

 

 

 

 

   CT Scans

 

F. CT Scans: Experience has been limited in the utilizatioof CT scans for the diagnosis of renal ab­scess. The attenuation coefficient nvalue (CT number) varies considerably with the amount of liquid pus or solid ndebris within the abscess, and abscesses cannot be differentiated from nhemorrhagic cysts or solid neo­plasms with certainty. Percutaneous needle naspiration of the mass under CT control may confirm the diag­nosis.

 

 

 

   CT Scans

 

 

 

 

G. Isotope nScanning: The rectilinear scan will depict a space-occupying lesion. With nthe use of technetium and iodine compounds, the Anger camera will show aavascular mass lesion. These findings also are compatible with simple cyst. nGallium-67 localizes in inflammatory tissue; an ab­scess will therefore n”light up” on dynamic scanning.

Gallium nscanning may demonstrate an abscess even when excretory urograms are normal.

Differential nDiagnosis

Iacute pyelonephritis, symptoms and signs may be similar to those of abscess; nhowever, no space-occupying lesion is shown on the urogram, and a gallium scawill not show an abscess.

Whesymptoms of vesical irritability are absent and urinalysis is normal, renal nabscess may be con­fused with acute cholecystitis. The presence of a pal­pable nand tender gallbladder may make the diagnosis. Radiographic visualization of nthe gallbladder and kid­neys should be definitive.

Acute nappendicitis may be confused with renal abscess, because renal pain ofteradiates to the lower abdominal quadrant. The findings on physical exami­nation, nlaboratory studies, and radiographic studies should allow differentiation.

At ntimes, renal cell carcinoma may be confused with renal abscess, especially whethere is fever re­lated to tumor necrosis. Radiographic studies and scans nusually will allow differentiation; however, per­cutaneous needle aspiratiomay be required in some cases.

Complications

Complications nof renal abscess include both bacteremia with generalized sepsis and rupture of nthe abscess into the perinephrium.

 

 

 

Treatment n             

 

In most npatients with acute focal or multifocal pyelonephritis, treatment with nappropriate antibiotics should produce a clinical response within one week of ninitiating therapy. However, well-established large abscesses are oftedifficult to treat with antibiotics alone, with most studies limiting treatment nof renal abscesses with antibiotics alone to lesions smaller than 3 cm.

 

In most npatients with suspected corticomedullary abscess, a prompt attempt at treatment nwith intravenous antibiotics directed against culture-specific bacteria iaddition to intravenous fluid resuscitation may be used. Medical treatment nalone should be limited to hemodynamically stable patients with small (< 3 cm) corticomedullary nabscesses. Patients with signs of hemodynamic instability due to sepsis or with nlarge renal abscesses (≥3 cm) should undergo percutaneous or surgical ndrainage for abscess management (see Surgical Care). Moreover, medical therapy nalone in the treatment of perinephric abscesses is inappropriate, as the risk nof mortality associated with perinephric abscess treated with antibiotics alone nis upward of 33%.

 

Intravenous nadministration of a penicillin derivative, a cephalosporin, an aminoglycoside, nor a fluoroquinolone is the appropriate initial medical treatment. Following nsufficient resolution of nausea/vomiting and fever, antibiotics may be nadministered orally.

 

For ncombination therapy, a beta-lactam antibiotic plus an aminoglycoside should be nadministered intravenously. Administer this line of therapy until culture and nsensitivity results are received and then modify the antimicrobial therapy to nthe most appropriate agent.

 

The nduration of therapy is not well defined. Continue parenteral antibiotics for at nleast 24-48 hours after patient symptoms clinically improve and the fever nresolves. Then, administer a suitable oral antibiotic medication and continue nthis treatment regimen for an additional 2-4 weeks, as determined by complete nclinical and radiographic resolution of the intrarenal process.

 

Factors nthat may contribute to medical treatment failure include elderly age, diabetes nmellitus, large abscesses, obstructive uropathy, and urosepsis.

Treatment ncalls for immediate intravenous administration of broad-spectrum antibiotics nand drainage of the abscess. The drainage technique depends on the size and nlocation of the abscess. Smaller, isolated lesions may be drained with a needle ninserted through the skin (percutaneous aspiration) under ultrasound guidance. nFor simple, one-cavity (unilocular) abscesses within the kidney, drainage is done nthrough a small tube (catheter drainage). If the abscess is large, located icertain areas of the kidney (renal cortex), or the patient is older and septic, nopen surgical drainage may be necessary. Sometimes it is not possible to save nthe kidney and removal of part or all of the kidney (simple, partial, or ncomplete nephrectomy) may be necessary.

 

Antimicrobial ntherapy alone is not indicated for patients with xanthogranulomatous npyelonephritis (XGP). Nephrectomy is required.

 

    NEPHROSTOMY

 

 

Drainage nby percutaneous means or surgical incision may be necessary. Relief of ncomplicating urinary obstruction is mandatory. Nephrectomy and partial nnephrectomy are required less often today than in the past.

 

 

Prognosis

The noutlook is good provided the diagnosis is made promptly and effective therapy nis instituted im­mediately.

 

 

 

PERINEPHRIC ABSCESS

 

Etiology

Perinephric nabscesses lie between the renal cap­sule and the perirenal (Gerota’s) fascia. nMost result from rupture of an intrarenal abscess into the perinephric space; nthe causative organisms are usually coliform bacteria and Pseudomonas, less noften staphylococci and obligate anaerobes.

Pathogenesis & nPathology

Staphylococcal nperinephric abscesses probably originate from rupture of a small renal cortical nabscess or, less commonly, from a renal carbuncle. The pri­mary renal lesiomay heal, although the perinephric abscess progresses.

Usually, however, nperinephric cellulitis and ab­scess complicate severe renal parenchymal ninfection caused by gram-negative bacteria in association with calcufous npyonephrosis or infected hydronephrosis. It is presumed that spontaneous nextravasation of infected material occurs. In this instance, pus and bacteria nusually are found in the urine.

Perinephric nabscesses may become quite large. When advanced, they tend to point over the niliac crest (Petifs triangle) posterolaterally.

 

Clinical Findings                           

A. Symptoms: The most common symptoms of perinephric abscess ninclude chills, fever, unilateral flank pain, and abdominal pain. Malaise and nprostra­tion occur variably. Only about one-third of patients complain of ndysuria.

B. Signs: Fever tends to be low-grade unless generalized nsepsis evolves. There is usually marked tenderness over the affected kidney and ncostovertebral angle. A large mass may be felt or percussed in the flank. nAbdominal tenderness accompanied by variable rebound tenderness may be nelicited. The diaphragm on the affected side may be elevated and fixed. nIpsilateral pleural effusion is common. Scoliosis with the concav­ity to the naffected side usually is seen; this results from spasm of the psoas muscle, nwhich also causes the patient to lie with the ipsilateral leg flexed on the nabdomen. Erythema and edeina of the overlying skin may be evident. Minimal nedema is best demonstrated by having the patient lie on a rough toweLfor a few nminutes.

 

C. Laboratory nFindings: Leukocytosis is usual but may be nmild; a shift to the left is commonly seen. The erythrocyte sedimentation rate nusually is elevated; anemia may be present. Pyuria and bacteriuria are found ncommonly but not routinely. Blood cultures may be positive. Unless bilateral nrenal disease is pres­ent, the serum creatinine and blood urea nitrogen values ngenerally are normal.

 

 Plaifilm (stoun in the left kidney)

 

D. X-Ray Findings: nA plain film of the abdomen typically shows evidence of a flank mass. nSurrounding edema often results in obliteration of the renal and psoas shadows non the affected side. Scoliosis with the concavity to the affected side is ncommon. The pres­ence of a calcified body in this area suggests an abscess nresulting from calculous pyonephrosis. Occasionally, a localized collection of ngas caused by infection with gas-forming (coliform) organisms may be observed nin the perirenal area.

       Excretory urogram

                                                      n

Excretory urograms nmay show delayed visualiza­tion or nonfunction related to obstructive uropathy nor parenchymal disease. Changes suggesting a space-occupying lesion (eg, ncarbuncle) may be noted; how­ever, evidence of advanced hydronephrosis or calcu­lous npyonephrosis is seen most commonly. Lack of mobility of the kidney with change nin position of the patient or with respiration strongly suggests acute or nchronic perinephritis. The entire kidney or only one pole may be displaced nlaterally by the abscess.

A barium enema may nshow displacement of the bowel anteriorly, laterally, or medially. Paralytic nileus may be observed on plain films of the abdomen or on upper ngastrointestinal series. Chest films may demonstrate an elevated dia­phragm othe ipsilateral side; fluoroscopy often shows fixation on respiration. Some nfree pleural fluid and platelike atelectasis may be observed.

When the findings nof excretory urography are equivocal, the performance of retrograde urograms nmay be helpful.

Gallium-67 nlocalizes in inflammatory tissue; hence, the diagnosis often may be confirmed nby use of the scintillation camera.

Echograms, CT nscans, and renal angiograms may assist in diagnosis, especially when combined nwith percutaneous needle aspiration.

 

Differential nDiagnosis

Acute renal ninfections cause many of the symp­toms that accompany perinephric abscess: nfever, lo­calized pain, and tenderness. In acute pyelonephritis, the urine nuniformly shows evidence of infection; in perinephric abscess, the urine may or nmay not show evidence of infection. X-ray studies and scans, how­ever, should nfacilitate differentiation of these 2 condi­tions.

Infected nhydronephrosis may cause fever and lo­calized pain and tenderness and may naccount for the presence of a flank mass. Again, x-ray studies and scans should nmake the differentiation.

Paranephric abscess nis a collection of pus external to the perirenal fascia and often is secondary nto in­flammatory disease of the spine (eg, tuberculosis). Many of the signs of nperinephric abscess may be seen on a plain x-ray film, but the finding of a nlesion in bone in the low thoracic area should suggest the correct diagnosis. nUrograms are normal.

Complications

Unless the correct ndiagnosis is made promptly and effective therapy is initiated early, the nmortality rate from generalized sepsis is quite high. Rarely, the perinephric nabscess may point just above the iliac crest posterolaterally or extend ndownward into the iliac fossa and inguinal region. It is most unusual for the nphlegmon to extend within the perirenal fascia across the midline to involve nthe opposite side of the body.

The abscess may nproduce considerable ureteral compression, giving rise to hydronephrosis. Eveafter drainage of the abscess, ureteral stenosis from periureteritis may evolve nduring the healing process.

Prevention

Early, effective ntreatment of urinary tract disease is the only means of preventing perinephric nabscess. Appropriate therapy of urinary tract infection and re­moval of calculi nand other obstructive conditions are of highest priority.

 

Treatment

Generally, ntreatment is similar to treatment for renal abscesses, except that surgical ndrainage usually is required for perinephric abscesses but may not be required nfor intrarenal abscesses. Intensive antimi­crobial therapy, based upon culture nand sensitivity testing of the pathogen isolated from urine, blood, or pus nobtained by needle aspiration of the lesion, is mandatory. Unless adequate npercutaneous drainage can be established, surgical drainage usually is needed. nBecause of underlying renal disease, nephrectomy may be required, either nacutely or subsequent to initial control of the abscess. Wheephrectomy is nnot required—indeed, even if the kidney itself is nor­mal—excretory urography nshould be performed about 3 montns after therapy is completed to make certaithat late complications (eg, ureteral stenosis) are not missed.

Prognosis

Perinephric abscess noften is fatal when diagnosis and appropriate therapy are delayed. A high index nof suspicion and improved methods of diagnosis and treatment should offer a nbetter prognosis than the 44% mortality rate observed by Thorley, Jones, nand San-ford (1974).

 

 

 

 

                                                                        TUBERCULOSIS   

 

Tuberculosis, or TB, primarily affects the lungs but the causative nbacteria, Mycobacterium tuberculosis, can spread to other parts of the body, nincluding the kidneys, bladder and urinary tract. Urinary tuberculosis caarise because the tuberculosis virus directly invades the kidneys or lower nurinary tract, or it can result from urinary system deposits of the proteiamyloid, formed when tuberculosis destroys other body tissues.   

 

Tubercle bacilli may invade one or more (or even all) nof the organs of the genitourinary tract and cause a chronic granulomatous ninfection that shows the same characteristics as tuberculosis in other organs. nUrinary tuberculosis is a disease of young adults (60% of pa­tients are betweethe ages of 20 and 40) and is a little more common in males than in females.

Etiology

The infecting organism is Mycobacterium tuber­culosis, nwhich reaches the genitourinary organs by the hematogenous route from the nlungs. The primary site is ofteot symptomatic or apparent.

The kidney and possibly the prostate are the pri­mary nsites of tuberculous infection in the genitourinary tract. All other ngenitourinary organs become involved either by ascent (prostate to bladder) or ndescent (kid­ney to bladder; prostate to epididymis). The testis may become ninvolved by direct extension from epididymal infection.

 

Pathogenesis

                                                  

A. Kidney and Ureter: When a shower of tuber­cle bacilli hits the renal cortex, the organisms nmay be destroyed by normal tissue resistance. Evidence of this is commonly seein autopsies of persons who have died of tuberculosis; only scars are found ithe kid­neys. However, if enough bacteria of sufficient viru­lence become nlodged in the kidney and are not over­come, a clinical infection is nestablished.

Tuberculosis of the kidney progresses slowly; it may ntake 15-20 years to destroy a kidney in a patient having good resistance to the ninfection. As a rule, therefore, there is no renal pain and little or no nclinical disturbance of any type until the lesion has involved the calices or nthe pelvis, at which time pus and or­ganisms may be discharged into the urine. nIt is only at this stage that symptoms (of cystitis) are manifested. The ninfection then proceeds to the pelvic mucosa and the ureter, particularly its nupper and vesical ends. This may lead to stricture and back pressure n(hydronephrosis).

As the disease progresses, a caseous breakdown of ntissue occurs until the entire kidney is replaced by cheesy material. Calcium nmay be laid down in the reparative process. The ureter undergoes fibrosis and ntends to be shortened and therefore straightened. This change leads to a n”golf-hole” (gaping) ureteral orifice, typical of an incompetent nvalve.

 

 

                

 

B. Bladder: Vesical nirritability develops as an early clinical manifestation of the disease as the nblad­der is bathed by infected material. Tubercles form later, usually in the nregion of the involved ureteral orifice, and finally coalesce and ulcerate. nThese ulcers may bleed. With severe involvement, the bladder be­comes fibrosed nand contracted; this leads to marked frequency. Ureteral reflux or stenosis nand, therefore, hydronephrosis may develop. If contralateral renal in­volvement noccurs later, it is probably a separate hema­togenous infection.

 

C. Prostate and nSeminal Vesicles:      

The passage of infected urine through the prostatic nurethra will ultimately lead to invasion of the prostate and one or both nseminal vesicles. There is no local pain.

On occasion, the primary hematogenous lesion in the ngenitourinary tract is in the prostate. Prostatic in­fection can ascend to the nbladder and descend to the epididymis.

D. Epididymis and nTestis: Tuberculosis of the prostate can extend along the vas or through nthe perivasal lymphatics and affect the epididymis. Because this is a slow nprocess, there is usually no pain. If the epididymal infection is extensive and nan abscess forms, it may rupture through the scrotal skin, thus establishing a npermanent sinus, or it may extend into the testicle.

Pathology

A. Kidney and Ureter: The gross appearance of the kidney with moderately advanced tuberculosis nis ofteormal on its outer surface, although it is usually surrounded by nmarked perinephritis. Usually, how­ever, there is a soft, yellowish localized nbulge. On section, the involved area is seen to be filled with cheesy material n(caseation). Widespread destruction of parenchyma is evident. In otherwise nnormal tissue, small abscesses may be seen. The walls of the pelvis, calices, nand ureter may be thickened, and ulceration appears frequently in the region of nthe calices at the point at which the abscess drains. Ureteral stenosis may be ncomplete, causing “autonephrectomy.” Such a kidney is fibrosed and nfunctionless. Under these circumstances, the bladder urine may be normal and nsymptoms absent.

Microscopically, the caseous material is seen as aamorphous mass. The surrounding parenchyma shows fibrosis with tissue ndestruction, small round cell and plasma cell infiltration, and epithelial and ngiant cells typical of tuberculosis. Acid-fast stains will usu­ally demonstrate nthe organisms in the tissue. Similar changes can be demonstrated in the wall of nthe pelvis and ureter.

In both the kidney and ureter, calcification is ncommon. It may be macroscopic or microscopic. Such a finding is strongly nsuggestive of tuberculosis but, of course, is also observed in bilharzial ninfection. Sec­ondary renal stones occur in 10% of patients.

In the most advanced stage of renal tuberculosis, the nparenchyma may be completely replaced by ca­seous substance or fibrous tissue. nPerinephric abscess may develop, but this is rare.

B. Bladder: In the early stages, the mucosa may be inflamed, but nthis is not a specific change. The bladder is quite resistant to actual ninvasion.

  Cystoscopy

 

Later, tubercles form and can be seen easily, nespecially through the cystoscope, as white or yellow raised nodules surrounded nby a halo of hyperemia. With severe vesical contracture, reflux may occur.

 

 

                      Yellow raised nodules surrounded by a halo nof hyperemia

 

 

Microscopically, the nodules are typical tuber­cles. nThese break down to form deep, ragged ulcers. At this stage the bladder is nquite irritable. With heal­ing, fibrosis develops that involves the muscle nwall.

 

C. Prostate and Seminal Vesicles: Grossly, the exterior surface of these organs may show nnodules and areas of induration from fibrosis. Areas of necrosis are common. Irare cases, healing may end in calcifica­tion. Large calcifications in the nprostate should suggest tuberculous involvement.

 

D. Spermatic Cord, Epididymis, and Testis: The vas deferens is often grossly involved; fusiform nswellings represent tubercles. The epididymis is en­larged and quite firm. It nis usually separate from the testis, although occasionally it may adhere to it. nMicroscopically, the changes typical of tuberculosis are seen. Tubular ndegeneration may be marked.

The testis is usually not involved except by direct nextension of an abscess in the epididymis.

 

 

 

Clinical Findings                             

                              

Tuberculosis of the genitourinary tract should be nconsidered in the presence of any of the following situations: (1) chronic ncystitis that refuses to respond to adequate therapy, (2) the finding of pus nwithout bac­teria in a methylene blue stain or culture of the urinary sediment, n(3) gross or microscopic hematuria, (4) a nontender, enlarged epididymis with a nbeaded or thickened vas, (5) a chronic draining scrotal sinus, or (6) ninduration or nodulation of the prostate and thickening of one or both seminal nvesicles (especially in a young man). A history of present or past tuber­culosis nelsewhere in the body should cause the physi­cian to suspect tuberculosis in the ngenitourinary tract when signs or symptoms are present.

The diagnosis rests upon the demonstration of tubercle nbacilli in the urine by culture. The extent of the infection is determined by n(1) the palpable findings in the epididymides, vasa deferentia, prostate, and nseminal vesicles; (2) the renal and ureteral lesions as revealed by excretory nurograms; (3) involvement of the bladder as seen through the cystoscope; (4) nthe degree of renal damage as measured by loss of func­tion; and (5) the npresence of tubercle bacilli in one or both kidneys.

 

A. Symptoms: There nis no classic clinical picture of renal tuberculosis. Most symptoms of this ndisease, even in the most advanced stage, are vesical in origin (cystitis). nVague generalized malaise, fatigability, low-grade but persistent fever, and nnight sweats are some of the nonspecific complaints. Even vesical ir­ritability nmay be absent, in which case only proper collection and examination of the nurine will afford the clue. Active tuberculosis elsewhere in the body is found nin less than half of patients with genitourinary tuberculosis.

 

1. Kidney and ureter – Because of the slow pro­gressioof the disease, the affected kidney is usually completely asymptomatic. Ooccasion, however, there may be a dull ache in the flank. The passage of a nblood clot, secondary calculi, or a mass of debris may cause renal and ureteral ncolic. Rarely, the presenting symptom may be a painless mass in the abdomen.

 

2. Bladder-The earliest symptoms of renal ntuberculosis may arise from secondary vesical in­volvement. These include nburning, frequency, and nocturia. Hematuria is occasionally found and is of neither renal or vesical origin. At times, particularly in a late stage of the ndisease, the vesical irritability may become extreme. If ulceration occurs, nsuprapubic pain may be noted when the bladder becomes full.

 

3. Genital tract-Tuberculosis of the prostate and nseminal vesicles usually causes no symptoms. The first clue to the presence of ntuberculous infection of these organs is the onset of a tuberculous nepididymitis.

Tuberculosis of the epididymis usually presents as a npainless or only mildly painful swelling. An ab­scess may drain spontaneously nthrough the scrotal wall. A chronic draining sinus should be regarded as ntuberculous until proved otherwise. In rare cases, the onset is quite acute and nmay simulate an acute nonspecific epididymitis.

Dysuria

Dysuria means painful or difficult urination. Urinary ntuberculosis can cause a burning or gripping sensation during urination. nPatients may feel an urge to urinate but be unable to. Many other conditions, nincluding a run-of-the-mill urinary tract infection, can cause dysuria, so this nsymptom is not helpful in diagnosing urinary TB.

Hematuria

Hematuria means blood in the urine. The urine might carry na pinkish tinge that the patient can identify as blood, or the contaminatiomight be visible only to a doctor checking urine under the microscope. Even a nfew drops of blood can discolor urine, so hematuria should not unduly worry the npatient. As with dysuria, many conditions other than urinary TB can cause nhematuria.

Pain

Patients with urinary TB typically complain of paialong the side between the last rib and the top of the hip, known as the flank. nFlank pain is a common sign in many conditions that affect the kidneys. nPatients often have back pain too, according to the Merck Manuals Online nMedical Library.

Abscess

Tuberculosis infection can spread from the kidney into nthe space surrounding it. The infection can spread to the psoas muscle, running nfrom the lower back to the thigh. Sometimes infection of the psoas causes aabscess on the front of the thigh.

Kidney Failure

According to Drs. Golden and Vikram in their November n2005 paper in “American Family Physician,” urinary tuberculosis nusually does not affect kidney function. The exception occurs with tuberculous ninterstitial nephritis, or inflammation in the spaces between the kidney ntubules, which interferes with filtration and can shut down the kidneys

 

 

B. Signs: Evidence nof extragenital tuberculosis may be found (lungs, bone, lymph nodes, tonsils, nintestines).               

 

 

                   n

 

1. Kidney-There is usually no enlargement nor tenderness of the involved kidney.

2. External ngenitalia-A thickened, nontender, nor only slightly tender epididymis may be discovered. The vas deferens often is nthickened and beaded. A chronic draining sinus through the scrotal skin is nalmost pathognomonic of tuberculous epididymitis. In the more advanced nstages, the epididymis cannot be differentiated from the testis upon palpation. nThis may mean that the testis has been directly invaded by the epididymal nabscess.

Hydrocele occasionally accompanies tuberculous nepididymitis. The “idiopathic” hydrocele should be tapped so that nunderlying pathologic changes, if pres­ent, can be evaluated (epididymitis, ntesticular tumor). Involvement of the penis and urethra is rare.

3. Prostate and seminal vesicles-These organs may be normal to palpation. Ordinarily, nhowever, the tuberculous prostate shows areas of induration, eveodulation. nThe involved vesicle is usually indurated, enlarged, and fixed. If epididymitis nis present, the ipsilateral vesicle usually shows changes as well.

C. Laboratory nFindings: Proper urinalysis af­fords the most important clue to the ndiagnosis of genitourinary tuberculosis.

1. Persistent pyuria without organisms on culture or non the smear stained with methylene blue means tuberculosis until proved notherwise. Acid-fast stains done on the concentrated sediment from a 24-hour nspecimen are positive in at least 60% of cases. How­ever, this must be ncorroborated by a positive culture.

About 15-20% of patients with tuberculosis have nsecondary pyogenic infection; the clue (“sterile” pyuria) is thereby nobscured. If clinical response to adequate treatment fails and pyuria persists, ntuber­culosis must be ruled out by bacteriologic and roentgenologic means.

2. Cultures for tubercle bacilli from the first nmorning urine are positive in a very high percentage of cases of tuberculous infection. nIf positive, sensitivity tests should be ordered. In the face of strong presump­tive nevidence of tuberculosis, negative cultures should be repeated.

The blood count may be normal or may show anemia iadvanced disease. The sedimentation rate is usually accelerated.

Tubercle bacilli may often be demonstrated in the nsecretions from an infected prostate. Renal function will be normal unless nthere is bilateral damage: as one kidney is slowly injured, compensatory nhypertrophy of the normal kidney develops. It can also be infected with ntubercle bacilli, or it may become hydronephrotic from fibrosis of the⁷bladder nwall (ureterovesical stenosis) or vesicoureteral reflux.

If tuberculosis is suspected, perform the tubercu­litest. A positive test, particularly in an adult, is hardly diagnostic; but a nnegative test in an otherwise healthy patient speaks against a diagnosis of ntuber­culosis.

 

D. X-Ray Findings: nA chest film that shows evidence of tuberculosis should cause the physiciato suspect tuberculosis of the urogenital tract in the presence of urinary nsigns and symptoms. A plain film of the abdomen may show enlargement of one nkidney or obliteration of the renal and psoas shadows due to perinephric nabscess. Punctate calcification in the renal parenchyma may be due to ntuberculosis.

 

            KUB

 

Plain Radiographs

Plan radiographs of the urinary tract are important nbecause they show calcification in the kidneys and in the lower genitourinary ntract. Ureteral calcification is very uncommon. Calcification rarely occurs ithe bladder wall and seminal vesicles except in advanced disease.

 

 

 

 

 

    

            Excretory urogram  

 

Intravenous nUrography (IVU)

 

High dose IVU has traditionally been the gold standard ntool to diagnose and evaluate genitourinary TB. It is still in practice but imany institutions has been replaced by spiral CT. IVU findings are distortioof calyx, ureteral dilation above a UVJ stricture or a rigid fibrotic ureter nwith multiple strictures. The cystographic phase of the IVU can give valuable ninformation about the condition of the bladder, which may be small and ncontracted (thimble bladder) or with filling defects.

 

Computed Tomography

 

Spiral CT has arguably replaced IVU as the imaging modality of nchoice for the diagnosis because of 3 dimensional reconstructed images. It is nequal to IVU in identifying calyceal abnormalities, hydronephrosis or nhydroureter, autonephrectomy, amputated infundibulum, urinary tract ncalcifications, and renal parenchymal cavities.

 

Ultrasonography

It is of limited value, though used for initial nscreening and follow up.   

 

Renal stones are found in 10% of cases. Calcificatioof the ureter may be noted, but this is rare. Small prostatic stones the size of ngrape seeds in the region of the pubic symphysis are ordinarily not due to ntuberculosis, but large calcific bodies may be.

Excretory urograms can be diagnostic if the lesion is nmoderately advanced. The typical changes include (1) a “moth-eaten” nappearance of the involved ulcer­ated calices, (2) obliteration of one or more ncalices, (3) dilatation of the calices due to ureteral stenosis from fibrosis, n(4) abscess cavities that connect with calices, (5) single or multiple ureteral nstrictures, with second­ary dilatation, with shortening and therefore nstraightening of the ureter, and (6) absence of function of the kidney due to ncomplete ureteral occlusion and renal destruction (autonephrectomy).

       Excretory urogram

 

If the excretory urograms demonstrate gross ntuberculosis in one kidney, there is no need to do a retrograde urogram on that nside. In fact, there is at least a theoretical danger of hematogenous or nlymphogenous dissemination resulting from the increased intrapelvic pressure.

 

        Retrograde nurography

 

 Retrograde urography may, how­ever, be carried out non the unsuspected side as a verifi­cation of its normality. This is further nsubstantiated if the urine from that side is free of both pus cells and ntubercle bacilli.

 

Retrograde npyelography

Indications: 1. stricture at the lower end of the nureter, 2. Ureteral catheterization to obtain urine samples for culture from neach kidney.

 

Percutaneous nAntegrade Pyelography

It is an alternative to retrograde pyelography to naspirate contents of the renal pelvis or from the tuberculous cavities to nestimate the quantity of drugs that has penetrated the walls.

It can also be used for percutaneous nephrostomy tube nplacement in an obstructive system.

 

Arteriography, Radioisotope Investigation, and nMagnetic Resonance Imaging are rarely indicated as they do not provide any nadditional information above imaging modalities.

 

 

 

E. Instrumental Examination:  Cystoscopy and Biopsy

 

Cystoscopy is rarely nindicated however in some place it is used in assessing the extent of disease nor the response to chemotherapy.

Biopsy is usually necessary nto rule out malignancy and is not advised before the initiation of medical ntherapy.

 

 Cystoscopic view

 

 Thorough cystoscopic study is indicated even when the noffending organism has been found in the urine and excretory urograms show the ntypical renal lesion. This will clearly demonstrate the extent of the disease. nCystoscopy may reveal the typical tubercles or ulcers of tuberculosis. Biopsy ncan be done if necessary. Severe contracture of the bladder may be noted. A cystogram nmay reveal ureteral reflux. A clean specimen of urine should also be obtained nfor further study.

 

  nClassification 

 I — nnondestructive (infiltrate) tuberculosis of kidney;

II — initial destruction (papillitis or small, by diameter about 1 cm, single cavity);

III —marked destruction (caverns or policavernosial tuberculosis one of kidney segments);

IV — total or subtotal destruction (policavernose tuberculosis of two segments, ntubercular pyonephrosis, calcification kidney).

They distinguish three forms of tuberculosis: ntuberculoinfiltrative, ulcerous and scar.

 

Classification

 

 

 

Diagnosis of Genitourinary Tuberculosis

 

Tuberculosis of the genitourinary tract should nbe considered in the presence of any of the following situations:

Chronic cystitis that refuses to respond to nadequate therapy,

The finding of pus without bacteria in a nmethylene blue stain or culture of the urinary sediment,

Gross or microscopic hematuria,

A nontender, enlarged epididymis with a beaded nor thickened vas,

a chronic draining scrotal sinus,

Induration or nodulation of the prostate and nthickening of one or both seminal vesicles (especially in a young man). A nhistory of present or past tuberculosis elsewhere in the body should cause the nphysician to suspect tuberculosis in the genitourinary tract when signs or nsymptoms are present.

The diagnosis rests on the demonstration of ntubercle bacilli in the urine by culture. The extent of the infection is ndetermined by:

The palpable findings in the epididymides, nvasa deferentia, prostate, and seminal vesicles,

The renal and ureteral lesions as revealed by nexcretory urograms;

Involvement of the bladder as seen through the ncystoscope

The degree of renal damage as measured by loss nof function,

The presence of tubercle bacilli in one or nboth kidneys.

 

 

 

 

 

 

 

 

 

 

Differential Diagnosis

               

   

Chronic nonspecific cystitis or pyelonephritis may nmimic tuberculosis perfectly, especially since 15—20% of cases of tuberculosis nare secondarily in­vaded by pyogenic organisms. If nonspecific infec­tions do nnot respond to adequate therapy, a search for tubercle bacilli should be made. nPainless epididymitis points to tuberculosis. Cystoscopic demonstration of ntubercles and ulceration of the bladder wall means tuberculosis. Urograms are nusually definitive.

Acute or chronic nonspecific epididymitis may be nconfused with tuberculosis, since the onset of tuber­culosis is occasionally nquite painful. It is rare to have palpatory changes in the seminal vesicles nwith nonspecific epididymitis, but these are almost routine findings ituberculosis of the epididymis. The pres­ence of tubercle bacilli on a culture nof the urine is diagnostic. On occasion, only the pathologist can make the ndiagnosis by microscopic study of the surgi­cally removed epididymis.

Amicrobic cystitis usually has an acute onset and is noften preceded by a urethral discharge. “Sterile” pyuria is found, nbut tubercle bacilli are absent. Cystoscopy may reveal ulcerations, but these nare acute and superficial. Although urograms show mild hydroureter and evehydronephrosis, there is no ulceration of the calices as seen in renal ntuberculosis.

Interstitial cystitis is typically characterized by nfrequency, nocturia, and suprapubic pain with vesical filling. The urine is nusually free of pus. Tubercle bacilli are absent.

Multiple small renal stones or nephrocalcinosis seeby x-ray may suggest the type of calcification seen in the tuberculous kidney. nIn renal tuberculosis, the calcium is in the parenchyma, although secondary nstones are occasionally seen.

Necrotizing papillitis, which may involve all of the ncalices of one or both kidneys or, rarely, a solitary calix, shows caliceal nlesions (including calcifications) that simulate those of tuberculosis. Careful nbacteriologic studies will fail to demonstrate tubercle bacilli.

Medullary sponge kidneys may show small calci­fications njust distal to the calices. The calices, how­ever, are sharp, and no other nstigmas of tuberculosis can be demonstrated.

In disseminated coccidioidomycosis, renal in­volvement nmay occur. The renal lesion resembles that of tuberculosis. Coccidioidal nepididymitis may be confused with tu­berculous involvement.

Urinary bilharziasis is a great mimic of tuber­culosis. nBoth present with symptoms of cystitis and often hematuria. Vesical ncontraction, seen in both diseases, may lead to extreme frequency. nSchistosomiasis must be suspected in endemic areas; the typical ova are found nin the urine; cystoscopic and urographic findings are definitive idifferential diag­nosis.

Complications

A. Renal nTuberculosis: Perinephric abscess may cause an enlarging mass in the flank. nA plain film of the abdomen will show obliteration of the renal and psoas nshadows. Sonograms and CT scans may be more helpful. Renal stones may develop nif secondary nonspecific infection is present. Uremia is the end stage if both nkidneys are involved.

B. Ureteral nTuberculosis: Scarring with stric­ture formation is one of the typical nlesions of tuber­culosis and most commonly affects the juxtavesical portion of nthe ureter. This may cause progressive hy­dronephrosis. Complete ureteral nobstruction may cause complete nonfunction of the kidney.

C. Vesical nTuberculosis: When severely dam­aged, the bladder wall becomes fibrosed and ncon­tracted. Stenosis of the ureters or reflux occurs, caus­ing hydronephrotic natrophy.

D. Genital nTuberculosis: The ducts of the in­volved epididymis become occluded. If nthis is bilat­eral, sterility results. Abscess of the epididymis may rupture ninto the testis, through the scrotal wall, or both, in which case the nspermatogenic tubules may slough out.

 

Treatment                

           

Tuberculosis must be treated as a generalized disease. nEven when it can be demonstrated only in the urogenital tract, one must assume nactivity elsewhere. (It is theoretically possible, however, for the primary nfocus to have healed spontaneously.) This means that basically the treatment is nmedical. Surgical excision of an infected organ, when indicated, is merely aad­junct to overall therapy.

A. Renal nTuberculosis: A strict medical regi­men should be instituted.

The following combinations of drugs can be utilized. nThe choice can be governed by the results of sensitivity tests. (1) nCycloserine, aminosalicylic acid (PAS), and isoniazid (INH). (2) Cycloserine, netham-butol, and INH. (3) Rifampin, ethambutol, and INH. The latter group is nprobably the most efficacious. The oral dose of each is as follows: nCycloserine, 250 mg twice daily; PAS, 15 g in divided doses; INH, 300 mg; nethambutol, 1.2 g; rifampin, 600 mg. Sensitivity test­ing may indicate the use nof streptomycin intramuscu­larly. Administer 1 g/d the first month, 1 g 3 times na week for the next month, and then 1 g twice a week. Since INH may cause nperipheral neuropathy, give pyridoxine, 100 mg/d orally. Wechsler and Lattimer n(1975) prefer the combination of INH, ethambutol, and Cycloserine.

While most authorities advise appropriate medi­catiofor 2 years (or longer if cultures remain posi­tive), Gow (1979) finds that a n6-month course of drugs is adequate. He recommends 600 mg of rifampin, 300 mg nof INH, 1 g of pyrazinamide, and 1 g of vitamin C daily for 2 months, followed nby 900 mg of rifampin, 1.5 g of pyrazinamide, and 1 g of vitamin C twice a week nfor 4 months.

If, after 3 months, cultures are still positive and ngross involvement of the affected kidney is radiologi-cally evident, nnephrectomy should be considered. Gow (1979) recommends that nonfunctioning nkidneys be removed after 1-2 months of medical therapy.

If bacteriologic and radiographic studies demon­strate nbilateral disease, only medical treatment can be considered. The only nexceptions are (1) severe sepsis, pain, or bleeding from one kidney (may nrequire ne­phrectomy as a palliative or lifesaving measure); and (2) marked nadvance of the disease on one side and minimal damage on the other (consider nremoval of the badly damaged organ).

B. Vesical nTuberculosis: Tuberculosis of the bladder is always secondary to renal or nprostatic tuber­culosis; it tends to heal promptly when definitive treatment nfor the ‘ ‘primary” genitourinary infection is given. Vesical ulcers that fail nto respond to this regi­men may require transurethral electrocoagulation. nVesical instillations of 0.2% monoxychlorosene (Clorpactin) may also stimulate nhealing.

Should extreme contracture of the bladder de­velop, it nmay be necessary to divert the urine from the bladder or perform subtotal ncystectomy and anas­tomose a patch of ileum or sigmoid to the remainder n(ileocystoplasty, sigmoidocystoplasty) in order to afford comfort.

C. Tuberculosis of nthe Epididymis: This is never an isolated lesion; the prostate is always in­volved nand usually the kidney as well. Only rarely does the epididymal infection break nthrough into the testis. Treatment is medical. If after months of treatment aabscess or a draining sinus exists, epididymectomy is indicated.

D. Tuberculosis of nthe Prostate and Seminal Vesicles: Although a few urologists advocate nremoval of the entire prostate and the vesicles when they be­come involved by ntuberculosis, the majority opinion is that only medical therapy is indicated. nControl can be checked by culture of the semen for tubercle bacilli.

E. General nMeasures for All Types: Optimal nutrition is no less important in treating ntuberculosis of the genitourinary tract than in the treatment of tuber­culosis nelsewhere. Bladder sedatives may be given for the irritable bladder.

F. Treatment of nOther Complications: Perinephric abscess usually occurs when the kidney is ndestroyed, but this is rare. The abscess must be drained, and nephrectomy nshould be done either then or later to prevent development of a chronic ndraining sinus.

 

    Nephrectomy n

 

 

 

 

 

                                                          Ureteroneocystostomy by Boary

 

Prolonged antimicrobial therapy is indicated. If nureteral stricture develops on the involved side, ureteral dilatations offer a nbetter than 50% chance of cure. The severely involved bladder may cause nincompetence of the ureterovesical junction on the uninvolved side. nUreteroneocystostomy cannot be done in such a blad­der; some form of urinary ndiversion may be required. For this reason, serial excretory urograms are neces­sary neven under medical treatment.

Prognosis

The prognosis varies with the extent of the disease nand the organs involved, but the overall control rate is 98% at 5 years. The nurine must be studied bacteriologically every 6 months during treatment and nthen every year for 10 years. Re­lapse will indicate the need for reinstitutioof treat­ment. Nephrectomy is rarely necessary. In the healing process, nureteral stenosis or vesical contraction may develop. Appropriate surgical nintervention may be necessary.

 

 

References:

a) basic nliterature:

1. Donald R. Smith, nM.D. General Urology, 11-th edition, 1984 p.177-244

2. Official Journal nof the European Association of Urology /2002-2007/.

3. Urological nGuidelines (European Assosiation of Urology) Health Care Office /august 2004 nedition/.

        4. nUrology. Infection diseases of genitourinary tract. Editors J. Lorens, J. nDembowski, R. Zdrojowy /Dolnoslaskie wydawnictwo edukacyyne, Wroclaw 2005, p.7-50

5. Scientific nFoundations of Urology. Third Edition 1990. Edited by Geoffrey D. Chisholm and nWilliam R. Fair, MD. Heinemann Medical Books, Oxford, p.123-152

b) supplementary nliterature:

1. Urinary Tract nInfection and Inflamation / Jackson E. Fowler, JR. MD. Year Book Medical nPublishers, Chicago 1989, p.138-165

       2. European Urology Supplements /2002-2007/.

       3. European Urology via nwww.eropeanurology.com

       4. Urology The Gold Jounal n/www.goldjournal/net/.

References of Tuberculosis:

1. Treatment of Tuberculosis: nGuidelines for National Programmes, 3rd ed. WHO, Geneva, 2003 n(http://www.who.int/docstore/gtb/publications/ ttgnp/pdf/2003.313.pdf).

2. Fain O, Lortholary O, nLascaux VV, Amoura II, Babinet P, Beaudreuil J, et al. Extrapulmonary ntuberculosis in the northeastern suburbs of Paris: 141 cases. Eur J Intern Med n2000;11:145–50.

3. Warren D, Johnson JR, nJohnsonCW, Franklin C. Lowe: Genitourinary TuberculosisCampbell’s Urology. 8th ned. Saunders; 2002.

4. Chattopadhyay A, Bhatnagar nV, Agarwala S, Mitra DK. Genitourinary tuberculosis in pediatric surgical practice. nJ Pediatr Surg 1997; 32:1283–6.

5. Chuang FR, Lee CH, Wang IK, nChen JB, Wu MS. Extrapulmonary tuberculosis in chronic hemodialysis patients. nRen Fail 2003;25:739–46.

6. Ferrie BG, Rundle JS. nGenitourinary tuberculosis in patients under twenty-five years of age. Urology n1985;25:576–8.

7. Queipo JA, Broseta E, nSantos M, Sanchez-Plumed J, Budia A, Jimenez-Cruz F. Mycobacterial infection ia series of 1261 renal transplant recipients. Clin Microbiol Infect n2003;9:518–25.

8. Lenk S, Schroeder J. Genitourinary ntuberculosis. Curr Opin Urol 2001;11:93–8.

9. Hemal AK, Gupta NP, Rajeev nTP, Kumar R, Dar L, Seth P. Polymerase chain reaction in clinically suspected ngenitourinary tuberculosis: comparison with intravenous urography, bladder nbiopsy, and urine acid fast bacilli culture. Urology 2000;56:570–4.

10. Missirliu A, Gasman D, nVogt B, Poveda JD, Abbou CC, Chopin D. Genitourinary tuberculosis: rapid ndiagnosis using the polymerase chain reaction. Eur Urol 1996;30:523–4.

11. Moussa OM, Eraky I, El-Far nMA, Osman HG, Ghoneim MA. Rapid diagnosis of genitourinary tuberculosis by npolymerase chain reaction and non-radioactive DNA hybridisation. J Urol n2000;164(2):584–8.

12. Fischetti G, Lombardo G, nBarrese F, Moello P, Cuzari S, Cristini C. Tb Test in the diagnosis of n‘‘closed’’ tuberculosis of the urinary tract. Minerva Urol Nefrol n1999;51(4):197–201.

13. Gow JG. Tuberculosis: ngenitourinary tuberculosis. Br J Hosp Med 1979;22:556–68.

14. Kao SC, Fang JT, Tsai CJ, Chen KS, nHuang CC. Urinary tract tuberculosis: a 10-year experience. Changgeng Yi Xue Za nZhi 1996;19(1):1–9.

15. Flechner SM, Gow JG. Role nof nephrectomy in the treatment of on functioning or very poorly functioning nunilateral tuberculous kidney. J Urol 1980;123:822–5.

16. The medical Letter: Drugs nfor tuberculosis. Treatment Guidelines from the Medical Letter 2004;28:83-88.

17. Wise GJ, Marella VK: nGenitourinary manifestations of tuberculosis. Urol Clin. North Am n2003;30:111-121.