Urinary Bladder Presentation

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BLADDERTRAUMA,INFLAMMATION,

TUMORS


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BLADDER TRAUMA

Introduction

Etiology

Pathology

Types of injury

Clinical features

Investigations

treatment


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BLADDER TRAUMA

The bladder is a pelvic hollow viscus whichmay be damaged as a result of a penetratinginjury to the lower abd, or through thecourse of pelvic surgery.


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AETIOLOGY

Road traffic accidents + pelvic fractures

Contact sports (blunt trauma)

Obstetric trauma.

Difficult hysterectomy

Spontaneous/idiopatic.


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PATHOLOGY

External injury to the emptybladder usually results in extraperitonealrupture.

When distended, injury usually results in intraperitonealinjury

In children below 6yrs, it is usually an intraperitonealinjury


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TYPES OF INJURY

Blunt injuries

Bladder contusion

Extraperitoneal rupture (80%; ant & lat parts)

Intraperitoneal rupture (20%; dome of bladder)

Open bladder injuries (stab, missiles)

Vesical fistulae

Vesico-vaginal

Vesico-cutaneous


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CLINICAL FEATURES

History of trauma

Lower abdominal pain

Hematuria

Suprapubic pain and swelling

Failure to pass any urine

Features of peritonitis(intraperitoneal)


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INVESTIGATIONS

Retrograde urethrocystogram: extravasation of contrast intoretropubic space or peritoneal cavity

Cystoscopy

IVU


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TREATMENT

Intraperitoneal rupture

Laparotomy

Suture tear in bladder

Urinary catheterisation for 7-10 days

Antibiotics

The duration between injury and repair determines mortality. Veryhigh if >48hrs


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Congenital anomalies:

Diverticula.

- Vesical diverticulum consists of a pouch-like evagination of the

bladder wall.

- commonly arise as congenital defects but more commonly as acquired lesions

caused by persistent urethral obstruction.

Exstrophy

- is a developmental failure in the anterior wall of the abdomen and the bladder,

so that the bladder either communicates directly through a large defect with

the surface of the body or lies as an opened sac.


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Miscellaneous Anomalies

Vesicoureteral refluxis the most common and serious anomaly. As a majorcontributor to renal infection and scarring (pyelonephritis).

Rarely, the urachus(the canal that connects the fetal bladder with the allantois)may remain patent in part or in whole. When totally patent, a fistulous urinarytract is created that connects the bladder with the umbilicus.


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Bladder Inflammation: CYSTITIS

A.k.a. inflammation of the urinary bladder

Affects all ages

Prevalence

Childhood

Females

Pregnancy

menopause


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CYSTITIS

cystitis

acute

Acutebacterial

Acute non-bacterial

chronic

Chronic

bacterial

Non-bacterial


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ACUTE BACTERIAL

Etiology: E. coli,Proteus vulgaris,P. aeruginosa, Strep faecalis, S.aureus, C. albicans, Klebsiellaspp

Routes

Ascending (p-papilla & p-papilla receptors)

Descending

Instrumentation

Blood

lymphatic


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PATHOLOGY Trigone and base are most commonly affected

Congested blood

Submucosal hemorrhages

Fibrinous or purulent discharge

Histology: leukocyte infiltration mucosal and submucosal oedema


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CLINICAL FEATURES

Frequency, urgency, dysuria, strangury

+/- hematuria

Chills, rigors, sweating.

Nausea, giddiness, tiredness Urine: foul odor and debris

Examination: nothing significant

Suprapubic tenderness


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INVESTIGATIONS

Urinalysismid stream urine (pus cells, proteinuria)

IVU- (bladder calculus, effects of BOO)

Cystoscopyreduced bladder capacity, hyperemia


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TREATMENT

Antibiotics. Empirically nitrofurantoin, nalidixic acid, septrin,cephalosporin. Then according to culture and sensitivity tests

Increase fluid intake

Alkalinise urine

Treat predisposing factors, sources of ascending and descendinginfections


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ACUTE NON-BACTERIAL CYSTITIS

chemical (formaldehyde, silver nitrate, CYCLOPHOSPHAMIDE)

Radiation

Mechanical (foreign bodies, bladder calculi)

Allergic ( drugs) ABACTERIAL PYURIA

TREATMENTSTOP / REMOVE IRRITATING AGENTTREAT SUPERINFECTION


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CHRONIC BACTERIAL CYSTITIS

Chronic inflammation with episodes of acute exacerbation

PATHOLOGY

{macro} Hyperplastic mucosa + bullous oedema {micro} Granulation tissue + macrophages + giant cells (sometimes in

the muscle layer)


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TREATMENT

Antibiotics. Empirically nitrofurantoin, nalidixic acid, septrin,cephalosporin. Then according to culture and sensitivity tests

Increase fluid intake

Alkalinise urine

Treat predisposing factors, sources of ascending and descending

infections

Antispasmodic agents, sedation and analgesics


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CHRONIC NON-BACTERIAL CYSTITIS

Tuberculous cystitis

Interstitial cystitis

Parasitic cystitis

Schistosomiasis

Trichomonal

Amoebic


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BLADDER TUMORS

Introduction

Epidemiology

Aetiology

Classification and staging Clinical features

Investigations

Complications

treatment


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INTRODUCTION

Benign tumors are rare

Bladder cancer is the 2ndmost common genitourinary neoplasm afterca prostate


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AETIOLOGY

Tobacco (carcinogenic arylamines e.g nitrosamine, 2-naphthylamine,4-aminobiphenyl)

Exposure to aniline and aromatic dyes, solvents, paints, leather dust,inks, rubber

Phenacetin abuse

Chemotherapy with cyclophosphamide (acrolein)

Schisosomiasis

Prior irradiation of the pelvis

Long term indwelling catheters (scc)

familial;- (no convincing evidence)*

TSG for p53 (xsome 17)- high grade& CIS

TSG for p16 (xsome 9)- low grade


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Classification and staging

Urothelial primary tumors

Transitional cell carcinoma Squamous cell carcinoma

Adenocarcinoma

Anaplastic ca

Non-urothelial primary tumors (rare)

Sarcoma, neurofibroma, small cell ca,

Secondary tumors (direct spread from prostate and cervix)


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Transitional cell carcinoma >90%

Commonest bladder tumor

Could be papillary(pedunculated) OR nodular(sessile)

Papillary: well-differentiated, low invasion

Nodular: poorly-diff, high invasion

TCCs are often multiple

Spread: direct> lymphatic >blood stream


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Squamous cell carcinoma


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Anaplastic ca

Rare

Poorly differentiated, infiltraion

Carcinomain-situ :

A flat non-invasive , HIGH GRADE urothelial carcinoma


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Non urothelial primary tumors

sarcomas

Rare (


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CLINICAL FEATURES

Gross hematuria- total/ terminal; intermittent

Symptoms of cystitis (when infection suprvenes)

Loin pain (hydroureters/hydronephrosis)

Weak stream, retentiion (involvement of bladder neck) Sloughs in urine (tumor necrosis)

Uni/ bi- lateral pedal edema (venous/ lymphatic occlusion)

Wt loss, malaise, severe anaemia, bone pain

Suprapubic mass (tumor/ urinary retention)

Palpable and tender kidneys (hydronephrosis

VE / DRE: mass at base of bladder

Bimanual exam under GA of tumor (findings correlate with clinicalstage of tumor)


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INVESTIGATIONS

Pcv (anaemia)

Urine C/S (infection)

Urine cytology: barbotage better than voided (tumour cells) flowcytometry (diploid better aneuploid)

Renal fxn test

IVU (hydronephrosis) X ray: chest, bones, calcification in bladder(schistosomiasis)

USSspread of tumor

CT scan, MRI (staging)

Cystoscopy Number - size Surface - condition of adjacent mucosa

position

Biopsy


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TREATMENT

Depends on

Degree of invasion

Cell type

Grade of differentiation

Accessibility Size and number of tumor

Age and clinical condition of patient


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T2 No/N1Mo

Partial cystectomy

Radical Radiotherapy + salvage cystectomy

Radical cystectomy + urinary diversions

T3 No/N1Mo

Radical Radiotherapy + salvage cystectomy

Radical cystectomy + urinary diversions

T4 N1Mo/M1

Radical Radiotherapy

Systemic chemotherapy

Neoadjuvant chemotherapy


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COMPLICATIONS

Hemorrhage/ anaemia

Cystitis / radiation cystitis /hemorrhagic

Hydronephrosis, hyrdroureter, renal failure

Urinary retention Fistulae

Limb oedema


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PROGNOSIS

Tis Ta T1 5yr survival rate 80-90%

T2-T3b 30-50%

T4 0%

Blacks worse prognosis

Women worse prognosis


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Urinary Bladder Presentation

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