The urinary tract (renal pelves, ureters, bladder, urethra) is lined by transitional epithelium (urothelium) with surface of flattened umbrella cells that have apical plaques of uroplakins.
Normal bladder wall is 3mm when distended, 5mm when collapsed. Volume = length x width x height x 0.52. Visualisation of ureteral jets confirms patency of the ureter. Bladder wall thickening (>5-6mm) may be associated with reduced bladder capacity, causes include:
- Bladder outlet obstruction – Muscle hypertrophy with wall thickening, then trabeculation with hypertrophy of individual muscle bundles. Crypts form, developing into diverticula. Acute obstruction causes marked enlargement with a thinned wall.
- Prostatic enlargement
- Neurogenic bladder
- Urethral stricture (congenital or inflammatory), posterior urethral valves
- Ectopic ureterocoele/cystocoele
- Tumours or blood clots
Extrinsic masses may displace or indent the bladder (may be pear-shaped), including lymphadenopathy, haemorrhage, pelvic lipomatosis, iliac artery aneurysm, tumours, psoas hypertrophy.
IV Urogram (IVU)
(IV pyelogram IVP, Excretory urography, XU). Administer intravenous contrast, 50mL Omnipaque 350 or urograffin 370.
- Control/preliminary films – Full length and tomogram of renal areas (8-11cm) to check for calcifications
- Instant/immediate nephrogram – Renal tomogram. Differing densities suggests renal artery stenosis. Irregular outlines suggests scar or mass/cyst (depending on density).
- 5 minute film of renal areas – To check for symmetrical excretion, detailed view of calyces. Persistent density/nephrogram suggests ureteric obstruction. Compression applied to distened pelvicalyceal systems.
- 15 minute film full length – On release of compression, demonstrating pelvicalyceal systems and ureters. Dilatation from obstruction, reflux or paralysed bladder. Displacement of the ureters by extrinsing masses or retroperitoneal fibrosis.
- 25 minute film – Pelvis to demonstrate distended bladder.
- Further delayed films up to hours ± prone films to check for the level of obstruction.
- Post micturition film – To demonstrate bladder emptying, drainage of dilated ureters.
Urinary Tract Obstruction
Dilated upper urinary tract (caliectasis, pyelectasis, ureterectasis). DDx peripelvic cyst.
- Obstructive uropathy (urinary tract obstruction, hydronephrosis) – Stone, stricture, tumour or extrinsic compression. The more proximal and chronic, the greater the dilatation; acute obstruction usually only causes mild dilatation. High pressure in the renal pelvis causes some reabsoption of filtrates via interstitium and lymphatics, also causes medullary ischaemia. Increasingly dense nephrogram with time, delayed contrast in urine. Pyelosinus reflux from rupture of fornix, due to contrast diuresis and hydrostatic pressure from obstruction. Obstruction increases risk of infection and stone formation. Unreleived -> irreversible cortical tubular atrophy, interstitial fibrosis. Causes include:
- Congenital anomalies – Posterior urethral valves, strictures, meatal stenoses, bladder neck obstruction, PUJ obstruction.
- Tumours – Prostate, bladder, ureter, pelvis, retroperitoneum, cervix/uterus.
- Inflammation – Prostatitis, ureteritis, urethritis, retroperitoneal fibrosis.
- Sloughed papilli or blood clots (usually <50HU, change in appearance over time).
- Pregnancy – Right > left.
- Uretrine prolapse, cystocoele
- Functional obstruction – Neurogenic abnormality of bladder/ureter including spinal cord injury, diabetic nephropathy.
- Pyonephrosis – Infection in obstructed kidney, can rapidly destroy renal parenchyma. Layering of echogenic pus and debris.
- Vesicoureteral reflux – In children from abnormal ureteral tunnel in VUJ; in adults from neurogenic bladder or bladder outlet obstruction. Chronic VUR causes reflux nephropathy.
- Congenital megaureter – Aperistaltic segment of lower ureter.
- Prune belly syndrome (Eagle-Barrett syndrome)
- Polyuria – From acute diuresis, diabetes insipidus etc.
Strictures are fixed narrowings, always associated with proximal dilatation. DDx active peristalsis, normal ureteric kink/bend.
- Post-traumatic/inflammatory – Surgery, instrumentation, previous stone causing scarring and fibrosis.
- Uroepithelial tumour – SCC, infiltrating type TCC.
- Extrinsic compression – Lymphoma, cervical carcinoma, colon carcinoma, endometriosis, Crohns, diverticulitis, PID.
(Urolithiasis, renal stone/calculus disease). 10% of the population develops a renal stone in a lifetime, M>F, peak 20-30yo, FHx. Stones form when the constituent exceeds the solubility (supersaturation), increased risk with low urine volume, dependent on urinary pH, deficiency of inhibitors of crystal formation in urine. May form in the renal calyces and pelvis or bladder.
- 70% are calcium oxalate or calcium phosphate (visible of XR).
- 15% struvite (magnesium ammonium phosphate, triple stones) – From alkaline urine (infection). Staghorn calculi are usually struvite, form in chronic infection (Proteus, some staphylococci).
- 10% uric acid stones – >50% don’t have hyperuricemia or hyperuricuria, ?due to pH <5.5 making uric acid insoluble.
- 1-2% cystine stones – Only in congenital cystinuria.
- Indinavir stones – Protease inhibitor for HIV. The only stone not dense on CT.
Complications include obstruction, ureteral stricture, chronic infection, loss of renal function. Typically oval or geometrical, tissue rim/halo sign (surrounding soft tissue ie ureter wall), proximal dilatation (ureter >3mm), renal oedema (hypodense and enlarged), perinephric stranding, perinephric fluid collection (forniceal rupture). DDx phleboliths (calcified venous thrombi) – round/oval up to 5mm with central lucency, <300HU, ‘tail sign’ (tubular tail representing the thrombosed vein). Ureteric calculi usually obstruct at the PUJ, pelvic brim or VUJ. Stones <6mm usually pass spontaneously within 6/52, larger stones usually require intervention.
Inflammation and Infection
Inflammation of the bladder wall from infection (bacteria, adenovirus, TB, schistosomiasis), drugs (cyclophosphamide), radiation, or autoimmune. Increased risk with bladder calculi, urinary obstruction, diabetes, instrumentation, immune deficiency. Bacteriuria is assymptomatic bacterial infection of the lower urinary tract without cystitis. Focal or diffuse bladder wall thickening, floating and layering debris in the urine, mucosa may be raised and hypoechoic/high T2 (oedema, inflammation), gas in bladder wall or lumen -> bright echoes with shadowing or ring-down artifact. Calcification may be from schistosomiasis, TB; radiation, chronic infection and cyclophosphamide cause curvilinear or flocculent calcification.
- Follicular cystitis – Lymphocytes aggregates into follicles within mucosa and wall. May not be associated with infection.
- Bullous oedema – Grape-like cysts elevating mucosa. Most associated with chronic irritation from catheters.
- Polypoid cystitis – Marked submucosal oedema causing urothelial projections, from bladder mucosa irritaiton (esp IDUC).
- Interstitial cystitis (chronic pelvic pain syndrome) – Chronic idiopathic inflammation of bladder without underlying infection, mostly women. Progressive reduction in bladder capacity, trabeculated fibrotic wall.
- Haemorrhagic cystitis – Haemorrhage in mucosa and submucosa from bacteria (esp when receiving cytotoxic chemotherapy) or adenovirus.
- Eosinophilic cystitis – Eosinophilic infiltration of unknown cause. Marked wall thickening, frequently nodular.
- Emphysematous cystitis – Gas in wall associated with poorly controlled diabetes, bladder outlet obstruction, E.coli (fement sugar in urine to form CO2 and H2. DDx instrumentation, vesicocolic fistula.
- Schistosomiasis (Schistosoma haematobium) – Common in Middle East esp Egypt. Lavae of blood fluke from infected water penetrates skin, enter lymphatics, mature in portal venous system. Adult females migrate and lay eggs in wall of bladder and ureter. Calcification of eggs embedded in wall of ureters and bladder. Ureters become aperistaltic causing VUR, bladder becomes fibrotic and contracted, fistulas to perineum/scrotum. May induce squamous metaplasia, increased risk of cancer (70% SCC, 30% TCC).
- Tuberculosis – Secondary infection to ureters and bladder (primarily kidneys). Calcification extending from proximal ureters to bladder (uncommon, patchy) causing wall thickening, contraction.
- Immunosuppressed – Candida albicans, less commonly cryptoccocus.
- Malacoplakia – Rare benign inflammatory soft yellow slightly raised 30-40mm mucosal plaques consisting of foamy macrophages, giant cells and lymphocytes. From chronic bacterial infection (esp E.coli, occasionally Proteus), increased risk with immunosuppression. Multiple smooth filling defects in distal ureter and bladder.
- Cystitis cystica – Nests of urothelium (Brunn nests) grown into lamina propria and creating multiple submucosal cysts. Most associated with infection. Often co-exists with glandularis (cystitis cystica et glandularis).
- Cystitis glandularis – Progression of cystitis cystica with transformation of Brunn nests into cuboidal or columnar epithelium with glands in lamina propria. Cysts of varying size, may obstruct ureteral orifice. May have intestinal metaplasia (NOT at increased risk of adenocarcinoma despite previous reports, unless associated with exstrophy).
- Squamous metaplasia – Response to injury.
- Leukoplakia – Rare squamous metaplasia with keratinisation and desquamation of uroepithelium from chronic UTI and stones. Irregular plaques, passage of flakes of desquamated epithelium in urine. Considered premalignant in the bladder, but not in the ureter.
Typically not associated with acute infection and is of no clinical significance.
- Ureteritis follicularis – Supepithelial lymphocytic aggregations causing fine granular elevations.
- Ureteritis/ureteropyelitis/pyeloureteritis cystica – Benign submucosal cysts from chronic UTI, haemorrhage. Multiple, small 2-3mm (up to 20mm in renal pelvis), smooth, round, filling defects in ureter/renal pelvis.
Blood clots are usually irregular, move with position, change size and appearance with time. Benign bladder tumours include leiomyoma, haemangioma, pheochromocytoma, neurofibroma; create smooth filling defects. Benign ureteric tumours are usually mesenchymal. Fibroepithelial polyps are small masses projecting into the lumen, in ureters, pelves or urethra.
(Urothelial carcinoma). M:F 3:1, 50-80yo, increased risk with arylamines (chemicals in textile and plastics), drugs (cyclophosphamide, phenacetin, long-term analgesics), chronic urinary stasis (eg horseshoe kidney), smoking, stones, Schistosomiasis, radiotherapy. Increased risk in diverticula. Bladder 50x more common than upper tracts, those with upper tract disease commonly have bladder TCC but in those with bladder TCC only 2-4% have upper tract disease.
- Papilloma – Benign, uncommon, usually younger patients. Most arise from lateral or posterior walls at bladder base. Small 5-20mm attached via stalk, lined by normal urothelium. Exophytic papillomas project into lumen and are attached via a stalk. Inverted papillomas extend into the lamina propria.
- Papillary urothelial neoplasm of low malignant potential (PUNLMP) – Papilloma with thicker urothelium or diffuse nuclear enlargement, tend to be larger. May recur.
- Papillary transitional cell carcinoma (TCC, most) – Confined to mucosa with exophytic polypoid with stalk, highly associated with multiplicity (in ~1/3) and recurrence. Stippled contrast filling in interstices of papilla, ‘champagne glass’/’goblet sign’ ureteral dilatation distal to filling defect (due to slow growth cf distal spasm with stone).
- Carcinoma in situ (CIS, flat TCC) – Malignat cells within a flat urothelium. May be area of thickening without an intraluminal mass. Commonly multifocal, may involve most of bladder surface extending into ureters and urethra. 50-75% progress to invasive cancer.
- Invasive TCC – 10% of low-grade and 80% of high-grade papillary TCC invade. May also develop from CIS. Nodular or flat, infiltrating through bladder wall, local invasion and metastases.
Iregular filling defect, tumour enhancement peaks at 60sec (earlier than normal bladder muscle). Colour Doppler shows vessels within the mass (cf blood clot). Isointense T1, slightly hyper T2 (cf bladder wall muscle). Calcifies in 5% (punctate or curvilinear). May be infiltrative segmentally invadingthe kidney. Metastases to LN, liver, lung, bone. DDx benign bladder wall thickening. Tx total nephroureterectomy and excision of cuff of bladder surrounding the VUJ.
- Ta – Noninvasive papillary.
- Tis – CIS.
- T1 – Into lamina propria.
- T2 – Into muscularis propria (detruser muscle).
- T3a – Microscopic extra-vesicle invasion.
- T3b – Gross extra-vesicle invasion, into perivesicular fat with shaggy iregular border, streaks in fat (DDx previous biopsy, inflammation, postradiation change).
- T4 – Invades adjacent organs.
Upper tract (renal pelvis and ureter) staging:
- Stage I – Limited to mucosa and lamina propria.
- Stage II – Invades into muscularis.
- Stage III – Beyond muscularis into periureteric/peripelvic fat or renal parenchyma.
- Stage IV – Invades adjacent organs or into perinephric fat.
Squamous Cell Carcinoma (SCC)
5% of uroepithelial tumours. Pure SCC is almost always associated with chronic infection (esp schistosomiasis) or irritation (calculi) esp diverticula. Mixed TCC/SCC more common. Most are infiltrative, superficial spreading, cause strictures, subtle filling defects, most have invaded bladder wall with metastases at time of diagnosis. Indistinguishable from TCC. Rarely calcifies (punctate or curvilinear). May be infiltrative, segmentally invading kidney.
Rare, most associated with bladder exstrophy or urachal remnant (90% of urachal carcinomas). Usually 40-70yo. Asymptomatic until local invasion or metastases.
Simple ureteroceoeles are congenital prolapse of dilated distal ureter into bladder lumen at normal insertion site, usually incidental. Small, oval into lumen at VUJ, fills and empties with ureteral peristalsis, ‘cobra head’/’spring onion’ (unopacified wall creates halo) is charactersitic. Ureteral jets seen.
Ectopic ureterocoeles usually associated with ureteral duplication. Variable sized projecting into lower bladder, posterior urethra, seminal vesicles, vas deferens, ejaculatory duct, vaginal vestibule or uterus. Remains unchanged in size after voiding. Distal ureter dilated and tortuous.
Mucosa herniated through defect in wall, most posterolateral near VUJ. Most acquired from bladder outlet obstruction (eg prostatic enlargement), occasionally congenital (maldeveloped muscle or outlet obstruction). Colour Doppler may show jet of urine from diverticular orifice with pressure to lower abdomen. Might not fill on cystogram, might not empty completely with voiding -> stasis -> infection and stones. May cause VUR, bladder outlet obstruction. Rarely develops TCC which tends to be a higher stage due to thinned overlying muscle.
Injury depends on amount of bladder filling at the time. Cystography or CT with at least 250mL bladder distension.
- Extraperitoneal bladder rupture (80%) – Puncture by pelvic fracture fragment. Extravasation into extraperitoneal retropubic space of Retzius, may extend into anterior abdominal wall, thigh, scrotum.
- Intraperitoneal rupture (20%) – Blunt trauma with rupture of dome. Extravasation into peritoneum. May mimic acute renal failure with reduced urine output, raised Cr (absorption of urine by peritoneum).
Chronic infection, pneumaturia, faecaluria. Barium enema and cystography detect the fistula in only 35%.
- Vesicocolonic – From diverticulitis (most common), colon/bladder carcinoma, UC, Crohns.
- Vesicovaginal – From gynaecological surgery (esp cervical carcinoma), occasionally obstetric injury.
- Vesicoenteric – Almost always Crohns.
Spastic or atonic. From meningomyelocoele, spinal trauma, diabetes, poliomyelitis, CNS tumour, MS. Prone to urinary stasis hence chronic infection, stones. Usually becomes trabeculated, thick-walled, reduced capacity.