RENAL Flashcards

Question

SOLID RENAL LESIONS Infiltrative lesions ill-defined, hypovascular and do not usually distort the renal contour

Answer 1

1. Urothelial carcinoma (aka TCC)—typically ill-defined and hypovascular, arises from the pelvicalyceal system and may obstruct or obliterate other calyces. May seed further down the urinary tract. Early tumours are seen as a mildly enhancing polypoid or sessile filling defect in the pyelographic phase on IVU, CT or MR. 2. Squamous cell carcinoma—usually associated with calculi or chronic UTI, can also occur in XGP. Starts as a plaque or stricture in the pelvicalyceal system but infiltrates the renal parenchyma early on, so there is usually a large parenchymal mass before any sizeable intrapelvic mass. May be very difficult to identify in chronically infected and distorted kidneys, e.g. in XGP. 3. Infiltrative subtypes of RCC—medullary carcinoma (nearly always in young patients with sickle cell trait) and collecting duct carcinoma both typically have infiltrative growth patterns and are aggressive, often metastatic at presentation. 4. Lymphoma*—usually secondary involvement in advanced NHL (primary lymphoma is very rare as there is no renal lymphoid tissue). Usually there are multifocal bilateral infiltrative hypovascular lesions on CT/MR, which are T2 hypointense, but can present as a single ill-defined mass, diffuse renal enlargement, perinephric soft-tissue thickening or direct extension from retroperitoneal lymphadenopathy. Can affect the renal sinus and mimic TCC. 5. Metastases—not uncommon, usually in the presence of metastatic disease elsewhere. Ill-defined hypovascular mass or masses. Lung, breast, GI tract, melanoma and the contralateral kidney are the most common sources. 6. Leukaemia—typically causes bilateral diffuse renal enlargement but can rarely present with single or multiple masses (chloroma in acute myeloid leukaemia). 7. Malakoplakia—uncommon inflammatory condition usually involving the urinary tract, related to recurrent E. coli infection. Most commonly involves the urothelium (causing nodules or plaques), but can also involve the renal parenchyma causing focal, multifocal or diffuse infiltrative lesions. May extend into the perinephric fat.Adrenals, urinary tract, testes and prostate 257 9 8. Sarcomas—rare. Angiosarcoma and rhabdomyosarcoma often have an infiltrative growth pattern. 9. Other rare lesions—e.g. plasmacytoma, extramedullary haematopoiesis, inflammatory pseudotumour, Wegener’s granulomatosis, Rosai-Dorfman disease, amyloidosis. 10. Mimics—focal pyelonephritis often presents as an ill-defined area of hypovascularity or striated enhancement, but the clinical features of sepsis are usually indicative. This is usually T2 hyperintense on MRI and may be hypo- or hyperechoic on US. A renal infarct presents as a peripheral wedge-shaped hypovascular area (± renal capsule enhancement) and may be multifocal. Predisposing factors are usually present. Radiation nephritis (due to spinal or retroperitoneal radiotherapy) presents as a well-defined wedge of hypoenhancement in the medial aspect of one or both kidneys.

Answer 2

1. Urothelial carcinoma—intraluminal filling defect on excretory urography, centred in the renal pelvis which secondarily invades the renal sinus and renal parenchyma. Commonly causes calyceal obstruction. 2. Squamous cell carcinoma—strongly associated with renal calculi and chronic UTI. 3. Metastasis to sinus lymph nodes. 4. Lymphoma*—may be limited to the renal sinus, particularly in PTLD. Ill-defined hypovascular mass which characteristically does not cause obstruction. 5. Mesenchymal tumour—e.g. lipoma, medullary fibroma, haemangioma, leiomyoma. 6. Retroperitoneal tumours extending into the renal sinus—any retroperitoneal tumour but lymphoma most commonly. 7. Renal parenchymal tumours projecting into the renal sinus

Answer 3

1. Peripelvic cyst—typically multiple and bilateral, arise from lymphatics within sinus fat. See Section 9.15. 2. Parapelvic cyst—single, larger cyst protruding into the sinus, originating from the adjacent parenchyma. See Section 9.15. 3. Sinus lipomatosis—echogenic central sinus complex on US. CT and MRI directly reveal fatty nature. 4. Vascular—renal artery aneurysm, AVM or renal vein varix can manifest as peripelvic lesions. Colour Doppler or contrast-enhanced CT are diagnostic. 5. Inflammatory—soft-tissue thickening in the sinus due to chronic/ severe pyelonephritis, XGP or malakoplakia. 6. Haematoma—due to anticoagulants or less commonly trauma. 7. Urinoma—due to pelvicalyceal rupture, usually associated with ureteral obstruction (e.g. stones), PUJ obstruction or trauma (including surgery). 8. Rare infiltrative disorders—any of the following can cause bilateral infiltrative masses in the renal sinus ± hydronephrosis. (a) Rosai-Dorfman disease*—renal involvement is rare but the most common manifestation is bilateral infiltrative renal hilar masses. (b) Retroperitoneal fibrosis—periaortic soft tissue may extend into the renal sinus. (c) Erdheim-Chester disease*—perinephric soft tissue may extend into the renal sinus.Adrenals, urinary tract, testes and prostate 259 9 (d) Amyloidosis*—can rarely involve the renal sinuses, causing infiltrative soft-tissue masses which may calcify (highly suggestive). (e) Extramedullary haematopoiesis—look for signs of bone marrow failure, e.g. bone sclerosis, splenomegaly. Uptake on sulphur colloid scintigraphy is diagnostic.

Answer 4

1. Lymphoma*—usually due to extension of renal/retroperitoneal lymphoma into perinephric space, but can present as isolated perinephric soft-tissue thickening. 2. Erdheim-Chester disease*—retroperitoneal involvement is common and produces a characteristic rind of soft tissue around the kidneys and aorta. 3. Amyloidosis*—may diffusely infiltrate the perinephric and retroperitoneal fat ± foci of calcification (highly suggestive). 4. Retroperitoneal fibrosis—periaortic soft tissue may extend into the perinephric space. 5. Metastases—most present as focal masses but breast cancer can present as infiltrative retroperitoneal soft tissue, which can involve the perinephric space. 6. Extramedullary haematopoiesis—can rarely infiltrate the perinephric fat. 7. Rosai-Dorfman disease*—can rarely cause subcapsular renal infiltration. 8. Nephroblastomatosis—only occurs in infants and children, due to persistent nephrogenic rests. Presents as bilateral confluent subcapsular soft-tissue nodules, which are homogeneous and hypovascular. Risk of malignant transformation to Wilms tumour

Answer 5

1. Renal lesions extending into the perinephric space—e.g. tumours (RCC, TCC), inflammatory lesions (malakoplakia, XGP). 2. Metastases—common sources include lung and melanoma. Usually in the presence of metastatic disease elsewhere. Lymphoma, leukaemia and myeloma may also rarely present as a focal perinephric mass. 3. Perinephric haematoma—may be spontaneous (due to vasculitis, anticoagulation or coagulopathy) or due to an underlying aneurysm or mass lesion, e.g. AML or RCC. Hyperattenuating subcapsular mass that does not enhance post contrast. 4. Nodular fat necrosis due to severe pancreatitis—usually presents with numerous small soft-tissue nodules (± central fat) throughout the intraabdominal fat. 5. Primary sarcoma—some liposarcomas may present as a solid mass. Other sarcomas can also arise from the perinephric space. 6. Other rare lesions not specific to the perinephric space—e.g. haemangioma, solitary fibrous tumour, Castleman disease, desmoid tumour, inflammatory pseudotumour, plasmacytoma.

Answer 6

1. Exophytic angiomyolipoma—often large, mimics perinephric liposarcoma. Features favouring AML include a focal renal cortical defect (representing the site of origin) and prominent intratumoural vessels extending into the renal parenchyma. 2. Liposarcoma—most common primary retroperitoneal malignancy, often arises from perinephric fat. Usually large and unencapsulated, displaces the adjacent kidney. See Section 4.4 for subtypes. 3. Perinephric lipomatosis—associated with renal stones and chronic renal infection (including XGP and TB). Expansion of the perinephric and renal sinus fat ± stranding. 4. Extraadrenal myelolipoma—can rarely arise from the perinephric space. Mimics liposarcoma due to mix of fatty and soft-tissue components, but typically appears encapsulated. Uptake on sulphur colloid scintigraphy suggests myelolipoma but is also seen in extramedullary haematopoiesis. 5. Extramedullary haematopoiesis—may contain foci of macroscopic fat.

Answer 7

1. Exophytic renal cyst or cystic lesions—including cystic neoplasms and abscesses. 2. Urinoma—due to pelvicalyceal rupture, usually associated with ureteral obstruction (e.g. stones), PUJO or trauma/surgery. 3. Lymphangiomatosis—rare benign lymphatic malformation resulting in bilateral multiloculated perinephric cysts and usually multiple bilateral peripelvic cysts

Answer 8

1. Global—nearly always due to main renal artery occlusion, either due to thrombosis, dissection or traumatic avulsion. Renal vein thrombosis can also give this appearance. A rim of capsular enhancement (‘rim nephrogram’) may be seen due to patent capsular vessels, usually developing several days after the initial vascular insult. 2. Segmental—due to focal renal infarction (usually embolic or vasculitic), focal pyelonephritis or an infiltrative lesion. A rim of capsular enhancement, if present, indicates infarction

Answer 9

1. Obstructive uropathy—e.g. ureteric stone/tumour. 2. Reduced arterial inflow—e.g. renal artery stenosis, Page kidney (reduced perfusion due to extrinsic compression by a subcapsular haematoma or collection). 3. Reduced venous outflow—e.g. renal vein thrombosis or compression. 4. Pyelonephritis—although a striated nephrogram is more common. As opposed to the other differentials, pyelonephritis does not result in a progressively hyperdense nephrogram.

Answer 10

1. Reduced arterial inflow—e.g. systemic hypotension/shock, and rarely bilateral renal artery stenosis. 2. Abnormal renal tubules—e.g. acute tubular necrosis (including iodinated contrast nephropathy), acute glomerulonephritis, acute papillary necrosis, tumour lysis syndrome or tubular protein deposition (myeloma, rhabdomyolysis, amyloidosis). In acute tubular necrosis the nephrograms may persist for days. 3. Bilateral obstructive uropathy—rare. 4. Reduced venous outflow—e.g. bilateral renal vein thrombosis. Rare

Answer 11

1. Acute ureteric obstruction. 2. Acute pyelonephritis—may be unilateral or bilateral. 3. Renal vein thrombosis. 4. Traumatic renal contusion

Answer 12

1. Acute pyelonephritis—may be asymmetrical. 2. Abnormal renal tubules—e.g. acute tubular necrosis, acute interstitial nephritis, tubular protein deposition (rhabdomyolysis, HIV nephropathy). 3. Hypotension/shock*.Adrenals, urinary tract, testes and prostate 263 9 4. Medullary sponge kidney—in the medulla only. Parallel or fan-shaped streaks radiating from the papilla to the corticomedullary junction (‘paintbrush’ appearance), representing dilated contrast-filled tubules. Nephrocalcinosis often also present. 5. Autosomal recessive polycystic kidney disease*—contrast medium in dilated tubules

Answer 13

1. Vasculitis—e.g. polyarteritis nodosa, Wegener’s granulomatosis, SLE, drug-induced. Causes multiple infarcts of differing ages due to occlusion of small intrarenal arteries. 2. Multiple emboli—usually from a cardiac source. 3. Pyelonephritis—less common than a striated nephrogram

Answer 14

Bilateral nonenhancing renal cortices with enhancement of the medulla and renal capsule. Pathognomonic for acute cortical necrosis, most commonly due to pregnancy-related complications (e.g. placental abruption, infected abortion, preeclampsia). Other causes include shock, sepsis, trauma, hyperacute transplant rejection, HUS, sickle cell disease, NSAIDs.

Answer 15

1. Paroxysmal nocturnal haemoglobinuria—most common cause. 2. Mechanical haemolysis—caused by malfunctioning prosthetic heart valves. 3. Severe sickle cell disease*—although haemolysis is predominantly extravascular (causing haemosiderin deposition in the liver, spleen and bone marrow), intravascular haemolysis can also occur in severe crises.264 Aids to Radiological Differential Diagnosis 4. Renal cortical necrosis—cortical thinning and low signal due to diffuse calcification.

Answer 16

1. Bilateral—in 85% multiple papillae are affected. Diabetes (50%), analgesics and sickle cell disease are the most important causes; others include trauma, acute tubular necrosis, shock (in infants) and chronic alcoholism. 2. Unilateral—usually due to obstruction, renal vein thrombosis, acute pyelonephritis or TB. 3. Papillae may show: (a) Enlargement (early) due to oedema. On CT, early disease presents as ill-defined areas of hypoenhancement in the papillary regions on the nephrographic phase. On US, echogenic rings may be seen in the medulla surrounded by a rim of fluid. (b) Partial sloughing—fissuring of the papilla occurs in one of two ways: (i) Central (medullary type)—a contrast-filled fissure forms at the tip of the papilla ± a central cavity (‘ball-on-tee’ or ‘egg-in-cup’ sign on excretory phase). (ii) Forniceal (papillary type)—fissuring occurs at the edges of the papilla causing a ‘lobster claw’ appearance—if this progresses it leads to total sloughing. (c) Total sloughing (signet ring sign)—the sloughed papillary tissue may: (i) Fragment and be passed in the urine. (ii) Cause ureteric obstruction. (iii) Remain free in a calyx as a filling defect (echogenic on US). (iv) Remain in the pelvis and form a ball calculus. (d) Necrosis in situ—the papilla is shrunken and necrotic but has not separated. This may then become calcified or ossified (particularly in analgesic nephropathy and TB). 4. Calyces—will appear dilated and clubbed following total sloughing of a papilla. On US this presents as a cystic cavity in the medulla contiguous with the calyces.

Answer 17

1. Renal artery stenosis—see Section 9.25. Note that other arterial abnormalities such as aneurysms and AVMs can also rarely cause renovascular hypertension. 2. Chronic bilateral parenchymal disease—e.g. glomerulonephritis, polycystic disease, diabetic glomerulosclerosis, connective tissue diseases (SLE, scleroderma, PAN), analgesic nephropathy. 3. Chronic reflux nephropathy or obstructive uropathy. 4. Tumours producing renin—characteristic in juxtaglomerular cell tumours (rare, seen in young adults), but can also occur with Wilms tumours and RCC. 5. Chronic renal infection—e.g. XGP, TB. 6. Renal vein thrombosis. 7. Radiotherapy.

Answer 18

1. Direct signs—seen at the site of narrowing. (a) Peak systolic velocity (PSV) in main renal artery >200 cm/s. Correlates well with >60% stenosis. (b) Renal artery PSV ÷ aortic PSV >3.5 correlates with >60% stenosis. (c) Turbulent flow in the poststenotic main renal artery.266 Aids to Radiological Differential Diagnosis (d) Lack of Doppler flow within main renal artery (indicates occlusion). 2. Indirect signs—seen distal to the site of narrowing. Less reliable than direct signs. (a) Tardus-parvus intrarenal waveform—blunted and delayed systolic upstroke, demonstrated by loss of the early systolic peak, a systolic upstroke gradient <3 m/s2 and acceleration time >0.07 s (time from onset of systole to peak systole). High specificity but low sensitivity. (b) Intrarenal arterial resistive index >0.8. (c) Smooth renal atrophy

Answer 19

1. Atherosclerosis—in ~75%, most commonly men >50 years. Bilateral in 30%. Stenosis of the proximal 2 cm of the renal artery is typical (± calcification); less frequently the distal artery or early branches at bifurcations. 2. Fibromuscular dysplasia—in ~20%, typically women <50 years. Nonatherosclerotic noninflammatory vasculopathy resulting in mural fibroplasia. Bilateral in 60%. Multiple stenoses ± dilatations, which may give the characteristic ‘string of beads’ appearance. Most commonly affects the middistal renal artery ± hilar branches, but can also involve carotid, vertebral and mesenteric arteries. 3. Renal artery dissection—usually due to extension of aortic dissection into the renal arteries, but can also occur due to trauma, instrumentation or spontaneously related to fibromuscular dysplasia, connective tissue disorders (Marfan and Ehlers-Danlos syndromes), severe atherosclerosis, malignant hypertension and extreme physical exertion. On imaging the dissection flap may be hard to visualize due to the small vessel size. Renal artery occlusion may also occur due to thrombosis or embolism. 4. Arteritis—PAN typically causes multiple intrarenal artery microaneurysms ± stenoses ± renal infarcts of different ages. SLE, Wegener’s granulomatosis and drug-induced vasculitis can cause a similar appearance. Takayasu arteritis can cause stenosis of the proximal renal artery. Other rare causes include radiation vasculopathy, thromboangiitis obliterans, syphilis and congenital rubella. 5. Renal artery entrapment—extrinsic compression of the renal artery by the diaphragmatic crus, due to an anomalous high origin of the renal artery. Usually presents in young patients. 6. Neurofibromatosis*—can rarely cause long tapered stenoses of the middistal renal arteries, usually seen in patients <50 years. 7. Midaortic syndrome—rare, seen in young patients. Causes long smooth narrowing of the suprarenal aorta ± renal artery involvement.Adrenals, urinary tract, testes and prostate 267 9 8. Extrinsic compression—by tumour, lymph nodes, aneurysm or RPF

Answer 20

1. Technical factors—incomplete filling during excretory urography. 2. Tumour—most commonly RCC (adult) or Wilms tumour (child). 3. Obstructed infundibulum—due to tumour, calculus or TB. 4. Duplex kidney—with a nonfunctioning upper or lower moiety. Signs suggesting a nonfunctioning upper moiety are: (a) Fewer calyces than the contralateral kidney. This sign is only reliable in unilateral duplication. (Calyceal distribution is symmetrical in 80% of normal individuals.) (b) A shortened upper calyx that does not reach into the upper pole and may be deformed by a dilated upper pole pelvis. (c) The kidney may be displaced downward or laterally by a dilated upper moiety pelvis. The appearances mimic a space-occupying lesion in the upper pole. (d) The upper pole may be rotated laterally and downward by a dilated upper moiety pelvis resulting in a ‘drooping lily’ appearance of the lower pole calyces. (e) The lower moiety ureter may be displaced or compressed by the upper pole ureter, resulting in a series of scalloped curves. (f) The lower moiety renal pelvis may be displaced laterally and its ureter then takes a direct oblique course to the lumbosacral junction. 5. Infection—abscess or TB. 6. Partial nephrectomy—± a surgical defect in the twelfth rib

Answer 21

1. Renal sinus masses—especially parapelvic and peripelvic cysts and benign mesenchymal tumours. These can indent and distort the pelvicalyceal system. 2. Vascular impression—intrarenal arteries can produce transverse or oblique compression lines, most commonly indenting an upper pole calyx ± calyceal obstruction (Fraley syndrome). Collateral vessels can also cause impressions, e.g. ureteric artery collaterals in RAS (indenting the renal pelvis) and venous collaterals in IVC obstruction or gonadal vein varices (indenting the ureter). Renovascular AVMs can also indent the renal pelvis. 3. Renal sinus lipomatosis—most commonly in older patients with chronic UTI or stones. Fat in the renal hilum produces a relative lucency on IVU and narrows and elongates the major calyces.

Answer 22

1. Early urothelial carcinoma—in practice any urothelial mass lesion is considered malignant until proven otherwise, due to the overlap in imaging findings. 2. Papilloma—most common benign ureteric tumour, can be solitary or multiple. Smooth surface, most commonly in distal ureter. Indistinguishable from early TCC and rare benign neoplasms, e.g. nephrogenic adenoma (caused by chronic inflammation), leiomyoma, neurofibroma, haemangioma, solitary fibrous tumour. 3. Pyeloureteritis cystica—due to chronic infection. Multiple 2–4-mm well-defined round submucosal cysts project into the lumen of the renal pelvis and/or ureter (upper > lower). 4. Metastases—rare, usually in the presence of disseminated disease. Lung, breast and GI sources are the most common. 5. Suburothelial haemorrhage—usually associated with coagulopathy or anticoagulants. Causes diffuse mural thickening ± filling defects in the renal pelvis and upper ureter. The thickening is hyperattenuating on unenhanced CT and does not usually cause significant obstruction, which can aid differentiation from TCC. 6. Endometriosis*—stricturing is more common but filling defects can occur, typically in the distal ureter. 7. Pseudodiverticulosis—multiple, usually bilateral, small (<5 mm) outpouchings from the upper-mid ureters. Associated with chronic UTI and obstruction, increased risk of malignancy. 8. Stevens-Johnson syndrome—can cause multiple small mucosal bullae in both ureters with mucosal sloughing, which may cause Adrenals, urinary tract, testes and prostate 269 9 obstruction. On CT there may be diffuse urothelial enhancement. Diagnosis usually already known due to cutaneous features.

Answer 23

1. Urothelial carcinoma—most common in the distal ureter, often multifocal. Enhances on CT. 2. Squamous cell carcinoma—rare, strongly associated with chronic UTI and stones. 3. Renal cell carcinoma—infiltrative subtypes may invade the pelvicalyceal system. 4. Squamous metaplasia—associated with chronic infection or calculi. Most common in the bladder and renal pelvis. Premalignant lesion, indistinguishable from tumour. 5. Tuberculosis*—causes nodular wall thickening and strictures. 6. Malakoplakia—granulomatous reaction to chronic E. coli infection; causes single or multiple urothelial plaques, nodules or masses indistinguishable from malignancy. 7. Amyloidosis*—can cause focal urothelial thickening and irregular filling defects ± calcification (highly suggestive). 8. Sarcoidosis*—can rarely cause a ureteric filling defect (granuloma)

Answer 24

1. Calculus. 2. Blood clot—due to trauma, tumour or bleeding diathesis. May be adherent to the wall or free in the lumen. Hyperattenuating on unenhanced CT. Changes in size or shape over several days. 3. Air bubble—see Section 9.38. 4. Sloughed papilla—due to papillary necrosis. Often triangular, may be rim-calcified. Look for blunted papillae in kidney. 5. Benign fibroepithelial polyp—rare, usually in the renal pelvis or ureter in young adults. Elongated, smooth and pedunculated—the stalk may be long, so the polyp can mimic an intraluminal lesion and may protrude into the bladder. Enhances on CT. 6. Fungus ball—typically in the renal pelvis, due to aspergillosis or candidiasis in immunocompromised patients

Answer 25

1. Pyelosinus backflow—contrast extravasation from fornix rupture into the renal sinus ± perinephric space. Contrast may also track inferiorly alongside ureter. 2. Pyelotubular backflow—physiological reflux of contrast from the calyx into the terminal portions of collecting ducts in the renal papilla (not due to forniceal rupture). Fan-like streaks from a calyx into the medullary pyramid. 3. Pyelointerstitial backflow—forniceal rupture into the renal interstitium; contrast flows from a calyx into the medullary pyramid ± renal cortex. More amorphous than pyelotubular. 4. Pyelolymphatic backflow—forniceal rupture into renal sinus lymphatics; contrast flows into small serpiginous lymphatic channels extending medially towards paraaortic lymphatics. 5. Pyelovenous backflow—forniceal rupture into arcuate or interlobar veins, with contrast flowing into the renal vein.

Answer 26

1. Stricture—due to tumour, calculus or TB. 2. Xanthogranulomatous pyelonephritis—typically there is a large calculus in a contracted and thickened renal pelvis, with gross calyceal dilatation and parenchymal atrophy. 3. Infiltrative processes of the renal sinus—these can constrict the renal pelvis and cause calyceal dilatation (see Section 9.19).Adrenals, urinary tract, testes and prostate 271 9 4. Extrinsic compression by an artery—most commonly a right upper pole calyx (Fraley syndrome). The renal pelvis is normal. 5. Calyceal diverticulum (mimic)—congenital outpouching that communicates with a calyceal fornix via a thin isthmus. May contain milk of calcium or dependent calculi (highly suggestive of a diverticulum).

Answer 27

1. Chronic reflux or obstruction—generally all the calyces are affected + associated parenchymal atrophy. The renal pelvis may be mildly dilated. 2. Papillary necrosis—clubbed calyces due to sloughing of papillae. See Section 9.23. 3. Congenital megacalyces—dilated and clubbed calyces (due to hypoplasia of medullary pyramids) usually with a normal renal pelvis. Number of calyces is often increased (polycalycosis) up to 20–25 (normal 8–12). Normal cortical thickness and good renal function differentiate it from chronic reflux/obstruction.

Answer 28

1. Congenital PUJ obstruction—due to abnormal embryogenesis of the PUJ resulting in a variable degree of stenosis. Often presents in childhood (or detected antenatally), but can present in adults. Extrinsic crossing vessels at the PUJ may contribute to obstruction. 2. Acquired PUJ obstruction—due to malignant and benign strictures, calculus (and other filling defects), previous trauma or inflammation. 3. Peripelvic cysts (mimic)—can be hard to differentiate from hydronephrosis on US. Excretory phase CT is diagnostic.

Answer 29

1. Oedema or stricture due to calculus—the calculus may have passed. 2. Primary tumour—TCC, papilloma and other benign and malignant neoplasms (see Section 9.27). 3. Metastasis—can present as a thick-walled stricture. Usually in the presence of disseminated disease. Lung, breast and GI sources are the most common. 4. Postsurgical—e.g. a misplaced ligature, following ureteric instrumentation or at a ureteral anastomosis. 5. Tuberculous stricture—typically multifocal stricturing causing a beaded or corkscrew ureter ± calcification. A particular hazard during the early weeks of treatment. 6. Schistosomiasis*—chronic disease causes distal ureteric stricturing ± calcification in the ureter or bladder (pathognomonic). 7. Ureterocoele—cystic dilatation of the ureter at the VUJ, projects into bladder. Due to congenital stenosis at ureteric orifice. Commonly associated with ectopic ureteric insertion (e.g. in duplex systems). Beware of a pseudoureterocoele due to an obstructing stone or mass at the VUJ. 8. Radiation ureteritis. 9. Malakoplakia—causes mural nodules and masses ± obstruction. 10. Amyloidosis*—can cause a ureteral stricture ± calcification (highly suggestive). 11. Vasculitis—e.g. PAN, Wegener’s granulomatosis, HSP, ChurgStrauss syndrome. Can rarely cause single or multiple ureteric strictures. 12. Primary obstructive megaureter—dilated pelvicalyceal system and ureter (>6 mm) transitioning to a normal calibre aperistaltic distal ureter, without a visible obstructing lesion. Congenital, often diagnosed antenatally but can present at any age. 13. Congenital midureteric stricture—short smooth stenosis in the midureter. Presents in infancy or antenatally, but is often mistaken for PUJ obstruction or megaureter

Answer 30

1. Retroperitoneal fibrosis—tethers and obstructs the midureters + medial deviation. Other infiltrative retroperitoneal processes can also obstruct the ureters but tend not to cause deviation, e.g. amyloidosis, Erdheim-Chester disease and extramedullary haematopoiesis. 2. Direct invasion of the ureter from pelvic and retroperitoneal malignancies—e.g. cervix, endometrium, bladder, prostate, rectum, lymphoma. 3. Stricture due to adjacent inflammation—e.g. appendicitis, diverticulitis, Crohn’s disease, tuboovarian abscess, pelvic actinomycosis, inflammatory AAA. 4. Endometriosis*—typically causes distal ureteric stricturing + other features on MRI. 5. Extrinsic compression from benign pelvic masses—e.g. large uterine fibroids, pelvic lipomatosis. 6. Retrocaval ureter—right side only. Dilated upper ureter with a transition to normal as the ureter courses medially behind IVC

Answer 31

Vesicoureteric reflux Dilated pelvicalyceal system and ureter down to the VUJ (as opposed to primary megaureter where the distal ureter is of normal calibre) + demonstrable reflux. The ureter may become very dilated and tortuous. See Section 14.61. No obstruction or reflux 1. Pregnancy—in the third trimester, R>L side. 2. Residual dilatation following relief of obstruction—most commonly following passage of a ureteric calculus or post prostatectomy. 3. Polyuria or diuresis—e.g. medication, diabetes insipidus. 4. Urinary tract infection—due to the effect of P-fimbriated E. coli on the urothelium. 5. Primary nonobstructive megaureter—similar to primary obstructive megaureter except there is usually no hydronephrosis

Answer 32

1. Normal variant—in 15%, due to large iliopsoas muscles displacing distal ureters medially. 2. Retroperitoneal fibrosis—medially displaced midureters. See Section 9.33. 3. Retrocaval ureter—the right ureter passes behind the IVC at the level of L4. The distal ureter lies medial to the dilated proximal portion. 4. Pelvic lipomatosis—nearly always in men, most common in Afro-Caribbeans. Medial displacement of the distal ureters with elevation and elongation of the bladder (‘pear-shaped’) and rectum + widened presacral space. Lucent on plain film, CT shows diffuse symmetrical fatty proliferation around bladder and rectum. 274 Aids to Radiological Differential Diagnosis May cause ureteric obstruction and cystitis glandularis. Chronic proctitis (e.g. due to UC or radiotherapy) can cause a similar appearance but the fatty proliferation is limited to the mesorectal fat. 5. Following abdominoperineal resection—the distal ureters are medially placed. 6. Pelvic sidewall mass—e.g. haematoma, lymphadenopathy, iliac artery aneurysm. Medially displaces one or both distal ureters

Answer 33

1. Hypertrophy of psoas muscles—can displace upper ureters laterally. 2. Retroperitoneal mass—e.g. lymphadenopathy, haematoma, abscess, lymphocoele, sarcoma, neurogenic tumours. Displaces upper ureters. 3. Pelvic mass—e.g. fibroids, ovarian tumour. Displaces distal ureters. 4. Aneurysmal aortic dilatation—displaces upper ureters. 5. Postoperative—e.g. urostomy, ureterolysis. 6. Prune-belly syndrome

Answer 34

1. Lymphoma*—most common. Confluent mass or masses of paraaortic/iliac lymph nodes, typically homogeneous and mildly enhancing on CT. Infiltrative, tends to surround vessels without causing significant narrowing. Often lifts the aorta away from the spine (‘floating aorta’ sign). Necrosis is rare except in very high-grade lymphomas. Calcification is rare except post treatment. 2. Other causes of retroperitoneal lymphadenopathy. (a) Metastases—common sources include kidneys, cervix, prostate and testes. Central necrosis, if present, aids differentiation from lymphoma. Extranodal retroperitoneal metastases can also rarely be seen, e.g. from lung cancer or melanoma, usually in the presence of metastatic disease elsewhere.Adrenals, urinary tract, testes and prostate 275 9 (b) Infection—e.g. TB or MAC. Nodes are typically necrotic. Most common in immunocompromised patients. (c) Sarcoidosis*—most commonly involves periportal nodes in the abdomen but paraaortic nodes can also be involved. Usually homogeneous, <2 cm and discrete (in contrast to the confluent adenopathy seen in lymphoma). (d) Castleman disease—benign lymph node hyperplasia. Presents as single or multiple avidly enhancing lymph node masses in the peripancreatic, paraaortic or iliac regions ± intratumoural vessels. Often homogeneous, may be heterogeneous if large ± calcification. (e) Rosai-Dorfman disease*—can rarely cause retroperitoneal adenopathy or masses. 3. Nonneoplastic masses and infiltrative disorders (a) Vascular malformations—retroperitoneal collateral veins are commonly seen in portal hypertension. IVC anomalies are occasionally seen (e.g. left-sided, double, azygos continuation). Congenital AVMs are rare, usually seen in the pelvis. Haemangiomas are very rare in the retroperitoneum but may show characteristic marked T2 hyperintensity on MRI ± peripheral or progressive enhancement. Phleboliths and peripheral interdigitating fat may also be seen. (b) Retroperitoneal fibrosis—see Section 9.33. (c) Erdheim-Chester disease*—characteristic rind of soft tissue around the aorta and kidneys. T1/T2 hypointense, minimal enhancement. (d) Extramedullary haematopoiesis—well-defined, heterogeneous soft-tissue masses ± fat, in a paravertebral or presacral location. Splenomegaly and diffuse skeletal changes (sclerosis in myelofibrosis, expansion in thalassaemia) are usually also present indicating bone marrow failure. (e) Amyloidosis*—infiltrative, poorly enhancing, soft-tissue mass or thickening that may be focal or diffuse throughout the retroperitoneum ± involvement of mesentery and omentum. T2 hypointense on MRI. Often contains characteristic coarse calcification. (f) Old rejected renal transplant—located in the right or left iliac fossa. Atrophic and poorly enhancing with areas of calcification, may mimic a tumour. Surgical clips and vascular anastomoses are indicative. 4. Sarcomas—many different types (most common are below). Often large, well-defined ± invasion of adjacent structures. Note that rhabdomyosarcoma is the most common sarcoma in children (very rare in adults). (a) Liposarcoma—most are characteristically fatty, but pleomorphic variants contain little or no fat, presenting as a nonspecific heterogeneously enhancing soft-tissue mass. 276 Aids to Radiological Differential Diagnosis Myxoid variants appear pseudocystic due to low attenuation on CT and high T2 signal on MRI, but internal reticular enhancement aids differentiation from true cysts. (b) Leiomyosarcoma—often shows extensive necrosis and cystic change. Intravascular extension, e.g. into the IVC, is a characteristic feature if present (although angiosarcoma can also do this). Calcification is rare. F>M. (c) Undifferentiated pleomorphic sarcoma—nonspecific heterogeneously enhancing mass. Calcification is not uncommon, and necrosis is usually less extensive than in leiomyosarcoma. M>F. 5. Neurogenic tumours—often occur in younger adults cf. sarcomas. Typically well-defined and usually benign but malignant varieties/transformation can occur. (a) Schwannoma—round/oval encapsulated mass, can be homogeneous (if small) or heterogeneous with areas of cystic degeneration and calcification (if large or ‘ancient’). Variable enhancement. Located along peripheral nerves, most commonly paravertebral ± nodular extension along the course of the nerve or towards a neural foramen. (b) Neurofibroma—round or plexiform in shape, located along peripheral nerves. Low attenuation on CT (20–25 HU) with only mild enhancement. On MRI the target sign is characteristic if present: peripheral T2 hyperintensity (myxoid component) + central T2 hypointensity (cellular component). Extension into a spinal neural foramen is also characteristic. Plexiform neurofibromas are diagnostic of NF1 and present as fusiform expansion of peripheral nerves, usually bilateral and symmetrical (most commonly involving the lumbosacral plexus). These are at higher risk of malignant transformation: significant asymmetry, progressive enlargement, irregular infiltrative margins, areas of necrosis or perilesional oedema are worrying features. (c) Paraganglioma—most common extraadrenal location is paraaortic distal to the inferior mesenteric artery origin (organs of Zuckerkandl). Typically shows avid enhancement on CT and MRI ± flow voids. May be homogeneously T2 bright or heterogeneous due to haemorrhage, necrosis and calcification. Uptake on MIBG scintigraphy is diagnostic. Typical clinical features (e.g. hypertension) may be present. Associated with NF1, MEN-2 and vHL. Risk of retroperitoneal haemorrhage. Up to 40% are malignant (large size and irregular margins are worrying features). (d) Ganglioneuroma—benign tumour arising from paravertebral sympathetic ganglia. Well-defined and lobulated, often extending around vessels without causing significant narrowing. May extend into neural foramina. Adrenals, urinary tract, testes and prostate 277 9 Homogeneously hypoattenuating on unenhanced CT (myxoid stroma) ± calcification. Heterogeneously T2 hyperintense on MRI ± characteristic whorled appearance. Heterogeneous delayed enhancement. Necrosis is rare. The more malignant ganglion cell tumours (neuroblastoma and ganglioneuroblastoma) nearly always occur in children. 6. Germ cell tumour—nearly always in men. Large lobulated paraaortic mass; homogeneous if seminoma, heterogeneous with haemorrhage and necrosis if nonseminomatous. Calcification and fat suggests teratoma (F>M). Most represent metastatic disease from a testicular primary, but the primary tumour may ‘burn out’, leaving only a testicular scar and a paraaortic mass—this tends to be ipsilateral to the primary testicular tumour, whereas primary retroperitoneal germ cell tumours tend to be centred on the midline. Elevated serum αFP or ß-HCG can aid differentiation from other heterogeneous tumours. 7. Desmoid tumour—benign but locally aggressive, with a high rate of recurrence. Heterogeneously enhancing infiltrative mass, may be T2 hyperintense (cellular) or hypointense (fibrotic). Often invades the abdominal wall, may encase and narrow vessels. Associated with Gardner variant FAP. 8. Solitary fibrous tumour—well-defined, lobulated, usually benign. Typically shows marked heterogeneous enhancement ± intratumoural vessels—these features are suggestive but can also be seen in paraganglioma (characteristic location ± clinical features), angiosarcoma (usually ill-defined ± intravascular extension) and Castleman disease (often more homogeneous). Cystic change, necrosis or haemorrhage can occur. Calcification is rare. 9. Undescended testis ± tumour—located along the expected course of testicular descent, most commonly close to the deep inguinal ring. Associated gonadal vessels and absence of the testis within the scrotum are pathognomonic. Increased risk of tumour development, usually presents when large. 10. Leiomyoma—rare, nearly always in women (often with a history of uterine leiomyomas); usually located in the pelvis. T2 hypointense on MRI ± areas of cystic change (particularly if large) ± intratumoural vessels (angioleiomyoma). May mimic leiomyosarcoma. 11. Primary sex cord stromal tumour—very rare, seen only in women (usually peri- or postmenopausal). Usually in the pelvis (broad ligament) but can rarely be higher in the retroperitoneum. Nonspecific, heterogeneous mass ± calcification. An elevated oestrogen level is suggestive. 12. Perivascular epithelioid cell tumour (PEComa)—very rare, usually in middle-aged women. Most are benign. Nonspecific, well-defined, heterogeneously enhancing mass.278 Aids to Radiological Differential Diagnosis 13. Extragastrointestinal stromal tumour—very rare. Nonspecific, well-defined, heterogeneously enhancing mass ± calcification. 14. Extramedullary plasmacytoma—very rare, most commonly perinephric in location. Nonspecific, infiltrative mass on imaging

Answer 35

1. Nonneoplastic cystic lesions—most common. (a) Pseudocyst—typically forms after an episode of acute pancreatitis; has a thick, enhancing wall and often heterogeneous contents ± foci of fat. Usually located close to the pancreas. A nonpancreatic pseudocyst can also rarely occur, representing a nonresolving, chronic haematoma. (b) Urinoma—occurs after rupture of the renal collecting system or bladder. Thin-walled, unilocular, located adjacent to the rupture site. May fill with contrast on delayed postcontrast images if there is an ongoing urine leak. (c) Lymphocoele—occurs after retroperitoneal lymphadenectomy due to leakage of lymph from cut lymphatics (look for surgical clips). Thin-walled, unilocular, located adjacent to iliac vessels or aorta. Fluid may have negative HU value on CT due to fat content. (d) Haematoma—most commonly due to coagulopathy; other causes include trauma and bleeding aneurysms or tumours (particularly AML and paraganglioma). Heterogeneous high attenuation on CT ± active contrast extravasation; if fluid–fluid levels are present (‘haematocrit’ sign) this indicates coagulopathy as the cause. (e) Abscess—enhancing wall, heterogeneous contents ± gas. Clinical features of sepsis. Common locations include perinephric, within psoas muscle and paravertebral (consider discitis). (a) to (d) can also become infected and resemble an abscess. If the abscess has a well-defined wall with minimal surrounding oedema/fat stranding, consider TB (cold abscess). 2. Lymphangioma—congenital malformation; can present at any age, more common in men (cf. items 3-8 below). Often large and elongated, characteristically traversing different compartments. Thin-walled, usually multilocular with no enhancement. May contain fat density/signal due to lymph. Calcification is rare except in lymphangiomatosis (multiple widespread lymphangiomas). 3. Cystadenoma—almost exclusively in women, can be mucinous or serous. Thin-walled unilocular cyst, usually in a lateral location. Solid nodules indicate malignant transformation to cystadenocarcinoma.Adrenals, urinary tract, testes and prostate 279 9 4. Epidermoid cyst—usually in the presacral space in middle-aged women, but can rarely be higher in the retroperitoneal space. Thin-walled, unilocular, typically near the midline. 5. Müllerian cyst—only occurs in women, typically obese with menstrual irregularity. Thin-walled, uni- or multilocular, usually in a lateral location. 6. Cystic mesothelioma—benign, most common in middle-aged women. Usually arises from the pelvic peritoneum but can rarely be retroperitoneal. Thin-walled, multilocular. 7. Cystic teratoma—benign, typically occurs in young girls. Complex cystic mass + characteristic foci of calcification and fat. 8. Lymphangioleiomyoma—cystic mass or masses with peripheral enhancement ± chylous ascites. Arises from lymphatics in the paraaortic region or next to iliac vessels. Only occurs in women with lymphangioleiomyomatosis, so look for the characteristic lung cysts. 9. Bronchogenic cyst—usually mediastinal, but can rarely be in the subphrenic retroperitoneal space. Thin-walled, unilocular, nonenhancing ± mural calcification. May be hyperattenuating due to proteinaceous contents. 10. Dilated cisterna chyli—located to the right of the aorta in the retrocrural space. Tubular, continues cranially as the thoracic duct. 11. Cystic change in a solid neoplasm—some solid tumours (such as paragangliomas, schwannomas, leiomyomas, leiomyosarcomas and synovial sarcomas) can show marked cystic change, becoming predominantly cystic with a thick irregular enhancing wall. Note that myxoid tumours appear pseudocystic, but the reticular internal enhancement (best seen on MRI) helps distinguish these from true cystic lesions. 12. Hydatid cyst—rare. Encapsulated, multilocular, no internal enhancement

Answer 36

1. Liposarcoma—usually large and unencapsulated, displaces and compresses the adjacent kidney. Contains a mixture of fat and soft tissue ± calcification. Amount of fat is variable: well-differentiated tumours are usually almost entirely fatty + thick fibrous septa; dedifferentiated tumours are fatty with nodular soft-tissue components >1 cm or foci of calcification; myxoid and pleomorphic variants contain little or no fat. 2. Angiomyolipoma—typically arises from the kidney but can be very exophytic or rarely completely extrarenal, mimicking a liposarcoma. Prominent intratumoural vessels or aneurysms and an associated cortical notch in the adjacent kidney indicate AML.280 Aids to Radiological Differential Diagnosis 3. Retroperitoneal fat necrosis—usually due to severe acute pancreatitis. Initially presents as ill-defined fat stranding, evolving into multiple fat-containing soft-tissue nodules, which involute over time. Can also involve mesenteric and omental fat. Long-term steroids can also cause fat necrosis but are more localized. Trauma or surgery can cause encapsulated fat necrosis: a thick, enhancing capsule and internal fat–fluid level are characteristic. 4. Perinephric lipomatosis—usually due to chronic infection or stones. Diffuse unencapsulated fatty proliferation with no soft-tissue components. A similar appearance can be seen with antiretroviral-associated lipodystrophy in patients with HIV. 5. Lipoma—rare in the retroperitoneum. Even a purely fatty retroperitoneal mass should be treated as suspicious for a well-differentiated liposarcoma. 6. Teratoma—rare, typically in young patients. Mature teratomas are encapsulated and contain a mixture of fat, soft tissue and calcification; a fat–fluid level is characteristic. Malignant teratomas usually contain little fat, and in men most represent metastases from a testicular primary (which may have ‘burned out’). 7. Hibernoma—rare, benign tumour of brown fat. Slightly higher attenuation than normal fat on CT (and slightly lower T1 signal on MRI) with internal septa ± enhancement. A prominent feeding vessel is almost pathognomonic. Typically shows high FDG uptake on PET (cf. well-differentiated liposarcomas, which show low grade uptake). 8. Extraadrenal myelolipoma—usually presacral, but can rarely arise higher in the retroperitoneum. Encapsulated fatty mass with streaky soft-tissue components. Can mimic liposarcoma but appears more well-defined and shows uptake on sulfur colloid scintigraphy. 9. Extramedullary haematopoiesis—haematopoietically inactive areas (yellow marrow) contain fat. 10. Others—paragangliomas, ganglioneuromas, haemangiomas and lymphangiomas can rarely contain macroscopic fat. Lipoblastomas appear similar to liposarcomas but occur only in infants and children.

Answer 37

1. Dense retroperitoneal/periaortic fibrotic soft-tissue mass (hypoechoic on US) that typically begins around the aortic bifurcation and extends superiorly to the renal arteries. Can rarely extend into the mesenteric root or into the pelvis. Reactive retroperitoneal lymphadenopathy is not uncommon. 2. Encases the aorta (usually sparing its posterior aspect and not displacing it away from the spine) and IVC, lymphatics and ureters ± obstruction. The ureters are tethered by the fibrosis and deviated medially. 3. In the acute inflammatory phase the mass shows moderate enhancement, T2 hyperintensity on MRI and uptake on PET. In the chronic fibrotic phase the mass shows minimal enhancement, T2 hypointensity and no uptake on PET.

Answer 38

1. Primary (‘idiopathic’)—>70%. Most cases now found to be autoimmune, due to IgG4-related disease. Similar histologically to chronic periaortitis and inflammatory AAA. 2. Secondary (a) Retroperitoneal malignancy—lymphoma and some metastases (e.g. from breast, stomach, colon, kidney, bladder, prostate, cervix, carcinoid, sarcomas) can trigger a desmoplastic reaction similar to RPF; lymphadenopathy tends to be more pronounced and metastases may be seen elsewhere. Malignancy often displaces the aorta away from the spine and may invade the psoas muscles or spine. Soft-tissue extension or adenopathy above the renal arteries is also suggestive of malignancy. (b) Retroperitoneal haemorrhage—e.g. due to ruptured aneurysm, trauma, surgery, coagulopathy. Blood incites a fibrotic reaction similar to RPF. (c) Inflammatory conditions—e.g. Crohn’s, diverticulitis, TB, histoplasmosis, actinomycosis, pyelonephritis and extravasation of urine. (d) Connective tissue diseases—e.g. ankylosing spondylitis, SLE, rheumatoid arthritis, PAN, Wegener’s granulomatosis, Churg-Strauss syndrome, sarcoidosis. (e) Other infiltrative retroperitoneal processes—particularly Erdheim-Chester disease, which characteristically causes a soft-tissue rind around the aorta (+ involvement of its posterior margin) and kidneys, usually sparing the ureters. Amyloidosis can also infiltrate the retroperitoneum but appears more diffuse than RPF, and does not usually involve the ureters. (f) Drugs—e.g. ergot derivatives, dopamine agonists, hydralazine, ß-blockers, analgesics. (g) Retroperitoneal radiotherapy

Answer 39

1. Calculus. 2. Foreign body—e.g. catheter, ureteric stent and other self-inserted objects. If chronic these can become encrusted with calcification. 3. Blood clot—hyperattenuating on unenhanced CT, no acoustic shadow on US, no vascularity or enhancement. If serpiginous in appearance, suggests bleed from upper urinary tract. 4. Ureterocoele—cystic dilatation of ureter projecting into the bladder at VUJ or ectopic insertion site, giving a ‘cobra-head’ appearance on IVU. 5. Fungus ball—in immunocompromised patients, due to candidiasis or aspergillosis

Answer 40

1. Malignant neoplasms—much more common than benign neoplasms. In practice all bladder polyps or masses are presumed malignant until proven otherwise, as imaging features overlap widely. (a) Urothelial carcinoma—accounts for 90% of bladder tumours in adults. Presents as a polypoid or papillary mass projecting into the lumen, or as an area of focal wall thickening and/or enhancement. Often multifocal, tends to recur. Invades perivesical fat ± adjacent organs in advanced cases. May have calcification along its surface. (b) Squamous cell carcinoma—<5% of bladder tumours, but >50% in areas where schistosomiasis is endemic. Other risk factors are chronic UTI and bladder calculi. Usually sessile and locally invasive, but otherwise indistinguishable from TCC. (c) Adenocarcinoma—<2% of bladder tumours, classically associated with a persistent urachus or bladder exstrophy. Presents as a focal mass/polyp or, in the signet ring variant, as diffuse bladder wall thickening (like linitis plastica). (d) Metastasis—most commonly from RCC, melanoma, breast or stomach. (e) Sarcoma—rare in adults, but rhabdomyosarcoma is the most common bladder tumour in children. Leiomyosarcoma is the most common bladder sarcoma in adults, usually large and invasive with areas of necrosis. (f) Lymphoma*—rare, secondary > primary. Usually a discrete nonspecific mass. (g) Neuroendocrine tumours—e.g. carcinoid tumour (small, polypoid) and small cell carcinoma (large, highly invasive and aggressive). Rare. (h) Melanoma—rare, may be T1 hyperintense on MRI. Can also arise in urethra. 2. Benign neoplasms. (a) Papilloma—usually small but essentially indistinguishable from papillary TCC. (b) Leiomyoma—submucosal in location, smooth and well-defined with homogeneous low T2 signal on MRI ± cystic areas. Can be hard to differentiate from well-differentiated leiomyosarcoma on imaging. (c) Neurofibroma—rare. Low attenuation on CT, T2 hyperintense on MRI + central hypointensity. May be focal, or diffuse/plexiform in NF1. (d) Paraganglioma—rare. Avidly enhancing mass ± ring calcification ± characteristic history of micturition-induced hypertension and headache. (e) Haemangioma—rare; small, hypervascular, homogeneously T2 bright. (f) Solitary fibrous tumour—rare; large, well-defined, heterogeneous enhancement. 3. Inflammatory lesions. (a) Nephrogenic adenoma—metaplastic response to chronic infection, stones, trauma or surgery. Usually solitary, can be polypoid or sessile. Does not invade muscularis or perivesical fat. Not premalignant, but often recurs. (b) Cystitis cystica and glandularis—metaplastic response to chronic infection, obstruction or stones, differentiating into either cystic lesions (cystica) or mucin-secreting glands (glandularis)—both often coexist. Cystitis cystica presents as multiple small submucosal cysts. Cystitis glandularis can present as an enhancing polypoid mass. Does not invade muscularis or perivesical fat. (c) Malakoplakia—uncommon chronic inflammatory response to E. coli infection, most often seen in the bladder. Variable appearances—solitary or multiple, polypoid or plaque-like, small or large, homogeneously or heterogeneously enhancing, intraluminal or invading perivesical fat. Indistinguishable from malignancy. (d) Inflammatory pseudotumour—rare, most often seen in young adults. Single heterogeneously enhancing mass, may invade perivesical fat. (e) Eosinophilic cystitis—rare. May present as diffuse bladder wall thickening or as a focal nonspecific enhancing mass. 4. Infection—TB and schistosomiasis. 5. Amyloidosis*—rare, but the bladder is the most common involved site in the urinary tract. Usually causes focal bladder wall thickening or mass ± characteristic mural calcification. 6. Ectopic prostate—rare congenital anomaly. Small intramural nodule usually in the trigone or urethra

Answer 41

1. Prostatic enlargement—median lobe often protrudes into the bladder base in benign prostatic hyperplasia (BPH). 2. Pelvic lymphadenopathy, mass or collection—indents bladder outline. Pelvic malignancies (e.g. prostate, cervix, rectum) may also directly invade the bladder. 3. Enlarged uterus—e.g. fibroids, pregnancy. Indents bladder dome. 4. Inflammation adjacent to the bladder—e.g. Crohn’s disease, diverticulitis. Causes focal bladder wall thickening adjacent to the inflammatory process. Intravesical gas suggests a fistula. 5. Iliac artery aneurysm—look for curvilinear calcification on XR. 6. Colonic distension. 7. Urachal cyst or mass—may indent the bladder dome in the midline. 8. Endometriosis*—most often seen on the serosal surface of the posterior bladder wall in the uterovesical pouch. Deposits can grow through the bladder wall and create filling defects. Typically T1 hyperintense on MRI due to haemorrhage + enhancement + other sites of involvement in the pelvis.

Answer 42

1. Any cause of cystitis—e.g. infection, haemorrhagic cystitis (e.g. due to radiation or chemotherapy—look for intraluminal blood clots), trauma, eosinophilic cystitis, interstitial cystitis. 2. Tuberculosis*—diffuse bladder wall thickening ± irregular mucosal masses in the acute phase. Contracted thick-walled bladder ± calcification in the chronic phase. Nearly always secondary to renal involvement, so the presence of normal kidneys practically excludes TB. 3. Schistosomiasis*—diffuse nodular bladder wall thickening in the acute phase, similar to TB except that infection starts in the bladder and progresses up the urinary tract. Diffuse bladder wall calcification ± contraction/fibrosis in the chronic phase. 4. Malakoplakia—can involve the bladder circumferentially

Answer 43

1. Chronic bladder outlet obstruction—e.g. due to BPH, urethral stricture, posterior urethral valves. Bladder is typically distended. 2. Neurogenic bladder (upper motor neuron damage only)— characteristic ‘pine cone’ appearance on cystogram in severe cases due to elongated and trabeculated bladder, which may be distended or small. Note that lower motor neuron damage and sensory neuropathy both lead to a distended, thin-walled bladder.

Answer 44

1. Signet-ring adenocarcinoma—‘linitis plastica’ appearance. 2. Metastases—from gastric cancer or leukaemia. 3. Lymphoma*—rare; 10% present as diffuse bladder wall thickening. 4. Plexiform neurofibroma—can diffusely involve the bladder wall. Low attenuation on CT, T2 hyperintense on MRI + central hypointensity. Rare; diagnostic of NF1

Answer 45

1. Calculus—may have passed through the ureter (typically <5 mm) or grown within the bladder (often large, round, may be laminated or spiculated). 2. Foreign body—encrustation of a ureteric stent or catheter balloon. 3. Tumour—e.g. TCC, SCC, paraganglioma, inflammatory pseudotumour. Typically surface calcification, so looks intraluminal on unenhanced CT (may be the only sign of an underlying tumour). 4. Alkaline-encrusted cystitis—due to Corynebacterium infection. Results in encrustation along infected urothelium. Can involve bladder or upper tracts

Answer 46

1. Schistosomiasis*—infrequent in the Western hemisphere but the most common cause of mural calcification worldwide. Thin curvilinear calcification outlining a bladder of (usually) normal size and shape. Calcification spreads to the distal ureters in 15%. 2. Tuberculosis*—rare and usually accompanied by calcification elsewhere in the urogenital tract. Contracted fibrotic bladder. 3. Chronic radiation or chemotherapy-induced cystitis—e.g. cyclophosphamide and mitomycin C. Contracted thick-walled bladder that can rarely calcify. 4. Tumour—mucinous adenocarcinoma may contain fine punctate calcification. Haemangioma may contain phleboliths. 5. Amyloidosis*—rare. Can cause focal bladder wall calcification

Answer 47

Congenital 1. Bladder exstrophy—extruded bladder communicating with skin surface (surgically corrected in infancy). Markedly widened pubic symphysis on plain film (manta ray sign). 2. Imperforate anus—high type. Rectum can fistulate with bladder or urethra. 3. Patent urachus—bladder communicates with umbilicus. Inflammatory 1. Diverticular disease—most common cause. 2. Crohn’s disease*. 3. Appendix abscess—and other pelvic sepsis. 4. Tuberculosis*—rare. Neoplastic 1. Carcinoma of the colon, bladder or reproductive organs. 2. Radiotherapy—usually 12–18 months after treatment. Trauma 1. Accidental. 2. Iatrogenic—particularly in obstetrics and gynaecology (vesicovaginal fistula).

Answer 48

1. Following instrumentation—e.g. catheterization or cystoscopy. 2. Vesicointestinal fistula—diverticular disease, Crohn’s disease and carcinoma of the colon or rectum. 3. Cystitis—due to gas-forming organisms and fermentation, especially in diabetics. Usually E. coli. Clostridial infections are rare, and usually secondary to septicaemia. 4. Penetrating wounds

Answer 49

1. Emphysematous cystitis—usually in diabetics

Answer 50

1. Any cause of gas in the bladder. 2. Ureteric diversion—into the colon or bladder. 3. Fistula—most commonly with colon or duodenum; other sites include stomach, small bowel, skin or vagina. Most commonly iatrogenic (e.g. nephrostomy, nephrolithotomy, hysterectomy); other causes include urinary calculi, XGP, TB, trauma, malignancy, radiotherapy, diverticulitis, Crohn’s disease or duodenal ulcer. 4. Emphysematous pyelitis—usually in diabetics. Gas may also be present in the renal parenchyma (emphysematous pyelonephritis) ± retroperitoneum

Answer 51

1. Congenital anomalies—due to incomplete involution. Any of these can be complicated by infection, stone formation or malignant transformation. (a) Patent urachus—the entire urachus remains patent, resulting in urine leaking from the umbilicus. Typically presents in neonates. (b) Urachal cyst—a focal portion of the urachus remains patent but does not communicate with the umbilicus or bladder, thereby forming a fluid-filled cyst. Unilocular with a thin minimally enhancing wall (unless infected).Adrenals, urinary tract, testes and prostate 289 9 (c) Urachal sinus—the umbilical end of the urachus remains patent, resulting in a blind-ending sinus extending inferiorly from the umbilicus ± intermittent discharge. (d) Vesicourachal diverticulum—the bladder end of the urachus remains patent, resulting in a midline outpouching from the anterosuperior bladder dome. 2. Infection—most common complication of urachal anomalies, most often by S. aureus and E. coli. Heterogeneous echogenicity on US, mural enhancement + surrounding fat stranding on CT. Can form an abscess ± fistula. May mimic urachal carcinoma if large and complex. 3. Malignancy—usually adenocarcinoma; most are mucinous with areas of calcification. Typically located adjacent to the bladder dome—a midline supravesical mass containing calcification is almost diagnostic of urachal carcinoma. Mucinous components will appear cystic on CT and T2 hyperintense on MRI. Solid components will enhance. Less common malignancies include TCC, SCC and sarcoma. 4. Benign tumours—e.g. adenoma, cystadenoma, fibroma, fibroadenoma, fibromyoma, hamartoma. Very rare, indistinguishable from carcinoma. 5. Mimics of urachal lesions. (a) At the umbilicus—an omphalomesenteric duct sinus can mimic an urachal sinus, although the former usually courses to the right (towards the distal ileum) rather than inferiorly in the midline. Other causes of periumbilical inflammation can mimic an infected urachal sinus. (b) Supravesical—other lesions inseparable from the bladder dome can mimic a urachal tumour or abscess, e.g. endometrioma, ovarian torsion, invasive bladder cancer, malakoplakia, inflammatory pseudotumour, peritoneal metastasis, appendiceal abscess, dropped gallstone

Answer 52

1. Diabetes mellitus—vast majority of cases. Bilateral and symmetrical linear calcification of the vas deferens wall. Ageing and secondary hyperparathyroidism can produce an identical appearance. 2. Chronic infection—mainly TB but also schistosomiasis, chronic UTI, gonorrhoea and syphilis. Vas deferens calcification is intraluminal and usually unilateral or asymmetrical. Seminal vesicles can show wall calcification in chronic schistosomiasis. 3. Seminal vesicle/ejaculatory duct calculi—rare, usually secondary to ejaculatory duct obstruction (e.g. congenital or due to chronic infection)

Answer 53

1. Benign calcification—typically located in the periurethral region or at the interface between transitional and peripheral zones. Most commonly due to chronic prostatitis (including TB and schistosomiasis) or BPH, but can also rarely be seen in hyperparathyroidism and may be extensive in alkaptonuria. 2. Prostate cancer—calcification within the peripheral zone is suggestive of underlying malignancy. 3. Impacted calculus in the prostatic urethra—located in the midline. 4. Seed brachytherapy—multiple tiny radioactive seeds implanted for treatment of prostate cancer. Very dense on plain film and CT. Radiation therapy can also cause prostate calcification

Answer 54

1. Testicular microlithiasis—multiple (>4) 1–3mm echogenic nonshadowing intratesticular foci, usually bilateral. Common incidental finding. No follow-up needed in low-risk asymptomatic patients. Note that solitary punctate calcification in an otherwise normal testis usually represents a phlebolith or sperm granuloma. 2. Scrotal pearl—represents a previously torted and detached testicular or epididymal appendix. Often mobile, located between the layers of tunica vaginalis. The appendix may also calcify in situ without detaching. 3. Previous trauma, torsion or infection—including TB. Calcification may be intratesticular or in the epididymis or tunica albuginea ± a chronic haematocoele or pyocoele. Missed torsion leads to an atrophic testis containing multifocal calcification. 4. Calcification in a mass lesion—Sertoli cell tumours and nonseminomatous germ cell tumours often contain calcification, especially those with a teratoma component. A ‘burned-out’ testicular tumour can regress into an irregular focus of calcification. Calcification can also be seen in the walls of cysts and epidermoids, and within paratesticular fibrous pseudotumours. 5. Sperm/suture granuloma—occurs at vasectomy site on vas deferens 6. End-stage renal failure—can produce bilateral epididymal calcification

Answer 55

1. Peyronie’s disease—the fibrous plaques on the tunica albuginea can calcify. 2. End-stage renal failure—can cause calcification of vessels or tunica albuginea in the penis.

Answer 56

1. Benign prostatic hyperplasia—most common prostatic mass. Presents as well-defined nodular enlargement of the transitional zone with heterogeneous T2 signal on MRI. May protrude into the bladder base. 2. Prostatic adenocarcinoma—95% of prostate cancers. 70% arise from the peripheral zone (in contrast to BPH). T2 hypointense on MRI + restricted diffusion + early enhancement and washout. Easier to detect in the peripheral zone (which is normally T2 hyperintense) than the transitional zone, where it can be hard to differentiate from BPH nodules—ill-defined margins, lentiform shape, homogeneous T2 hypointensity + restricted diffusion favours carcinoma. Tumours may show extracapsular invasion ± involvement of seminal vesicles, bladder, rectum or pelvic floor/ sidewall. Typically metastasizes to lymph nodes and bones (sclerotic deposits), and less commonly to lung and liver. 3. Benign mimics of prostate cancer (a) Postbiopsy haemorrhage—commonly seen in the peripheral zone, usually resolves after 6–8 weeks. Causes T2 hypointensity ± restricted diffusion, but the presence of T1 hyperintensity distinguishes this from cancer. (b) Prostatitis—acute, chronic and granulomatous (e.g. TB, malakoplakia, sarcoidosis) prostatitis all usually involve the peripheral zone, causing focal or diffuse T2 hypointensity + restricted diffusion indistinguishable from cancer. Granulomatous prostatitis can also extend beyond the prostate. Prostatitis can lead to necrosis and atrophy of the peripheral zone resulting in volume loss, T2 hypointensity and 292 Aids to Radiological Differential Diagnosis restricted diffusion. Volume loss and low-level enhancement can help differentiate this from carcinoma. (c) Normal structures—the anterior fibromuscular stroma (anterior to transitional zone) and central zone (around ejaculatory ducts) are both homogeneously and symmetrically T2 hypointense and must not be mistaken for carcinoma. 4. Secondary malignancy—usually due to direct prostate invasion from bladder or rectal cancer. Tumours of the prostatic urethra (e.g. carcinoma, melanoma) can also invade the prostate. Metastases (e.g. from lung, melanoma, GI tract) are less common. 5. Rare prostate neoplasms—serum prostate specific antigen (PSA) is usually normal. Bone metastases, if present, are usually lytic (in contrast to the sclerotic metastases seen in adenocarcinoma). (a) Other carcinomas—SCC, TCC and BCC can rarely arise from the prostate. SCC is T2 hypointense, indistinguishable from adenocarcinoma. TCC and BCC may be T2 hyperintense. SCC and TCC have a poor prognosis. (b) Sarcomas—most common are rhabdomyosarcoma (in children) and leiomyosarcoma (in adults). Usually much larger than adenocarcinoma and more heterogeneous on T2 and postcontrast sequences due to haemorrhage and necrosis. Often invades adjacent structures and metastasizes early. (c) Stromal tumour of uncertain malignant potential (STUMP)—well-defined heterogeneously enhancing solid-cystic mass, often large. Involves both peripheral and transitional zones (in contrast to BPH, which displaces the peripheral zone). May be adherent to rectum, often recurs after surgery. Can transform into stromal sarcoma. (d) Lymphoma*—homogeneous soft-tissue mass, which can involve the whole prostate. Usually secondary involvement, with disease present elsewhere. (e) Neuroendocrine tumours—e.g. carcinoid (low grade, heterogeneously T2 hyperintense), small cell carcinoma (high grade, very aggressive), paraganglioma (T2 hyperintense, avid enhancement, characteristic clinical picture of headache, tachycardia and sweating induced by micturition or rectal examination). 6. Rare benign lesions—e.g. inflammatory pseudotumour, solitary fibrous tumour, leiomyoma, neurofibroma, haemangioma, dermoid cyst. 7. Amyloidosis*—rare; T2 hypointense with no restricted diffusion and minimal enhancement

Answer 57

1. Midline—(a)-(c) are located posterior to the prostatic urethra and are unilocular and T2 bright on MRI, with variable T1 signal depending on protein content. Infection and stone formation can occur. (a) Utricle cyst—small (8–10 mm), does not extend beyond prostate. Communicates with prostatic urethra. May be associated with other congenital genitourinary anomalies. (b) Müllerian duct cyst—larger, elongated, usually extends above the prostate. Does not communicate with urethra. (c) Ejaculatory duct cyst—rare, due to obstruction and dilatation of ejaculatory duct. Usually small and paramedian, may appear in the midline if large. Can communicate with urethra, vas deferens and/or seminal vesicles. (d) Cowper’s duct cyst (mimic)—located inferior to the prostatic apex within the urogenital diaphragm or bulb of the corpus spongiosum. Usually unilocular, midline or paramedian. If large, may appear inseparable from the prostate. Usually communicates with the bulbous urethra. (e) TURP defect (mimic)—irregular periurethral urine-filled defect continuous with bladder lumen. 2. Lateral (a) Cystic degeneration of BPH—most common cystic lesion. Occurs in the transitional zone only. Usually small and multiple, may contain haemorrhage or calculi. (b) Retention cyst—also occurs in BPH but can be located in any zone. (c) Abscess—clinical features of acute prostatitis are key. Increased risk in diabetic or immunocompromised men. Irregular enhancing walls, heterogeneous contents ± septations + restricted diffusion. May rupture into urethra (creating a urethral pseudodiverticulum) or fistulate with the rectum. A tuberculous abscess may create multiple fistulae to the perineal and scrotal skin (‘watering can’ perineum). (d) Cavitary prostatitis—due to chronic prostatitis, resulting in cystic change throughout the gland (‘Swiss cheese’ appearance). (e) Cystic tumours. (i) Cystic prostate carcinoma—some variants of adenocarcinoma (e.g. mucinous or ductal) can show cystic change. Usually located in the peripheral zone (in contrast to cystic BPH). (ii) Multilocular cystadenoma—benign cystic tumour with multiple enhancing septations, typically very large and extending well above the prostate without invasion of adjacent structures. May contain haemorrhage and small enhancing solid elements. Often appears in the midline due to its large size. (iii) Lymphangioma—rare. Multiloculated, minimal enhancement. (f) Hydatid cyst—very rare. Encapsulated, multilocular, no internal enhancement

Answer 58

1. Congenital—often associated with other genitourinary tract anomalies. (a) Agenesis/hypoplasia—bilateral agenesis is associated with cystic fibrosis. Unilateral agenesis is often associated with ipsilateral renal agenesis. (b) Cyst—bilateral cysts are associated with ADPKD. A unilateral cyst (or cystic dilatation) is often associated with ejaculatory duct obstruction and ipsilateral renal agenesis—the triad of Zinner syndrome. The cyst may contain proteinaceous material (T1 hyperintense). A ureteric remnant is often present and may insert ectopically onto the cystic seminal vesicle or other sites. 2. Secondary tumour invasion—most commonly by prostate cancer (stage T3b disease), less commonly by bladder or rectal cancer. The vas deferens may also be involved. 3. Iatrogenic changes—prostate biopsy can cause seminal vesicle haemorrhage (intraluminal T1 hyperintensity helps differentiate this from malignant infiltration). Radiotherapy often causes bilateral symmetrical seminal vesicle atrophy with luminal narrowing or obliteration and diffuse mural T2 hypointensity. 4. Infection—usually secondary to prostatitis (e.g. bacterial, tuberculous, schistosomiasis). Diffuse mural thickening and enhancement with luminal dilatation in the acute phase. An abscess may form, particularly in diabetics or following instrumentation. In chronic or recurrent infection the seminal vesicles atrophy.Adrenals, urinary tract, testes and prostate 295 9 5. Amyloidosis*—common in the elderly. Bilateral diffuse T2 hypointense mural thickening and luminal narrowing. The lack of restricted diffusion or enhancement helps distinguish this from malignant infiltration. 6. Primary seminal vesicle tumours—very rare. Malignant tumours (infiltrative appearance) are more common and include adenocarcinoma, sarcoma and seminoma. Benign tumours (well-defined) include cystadenoma (multiloculated cystic mass), leiomyoma, fibroma, schwannoma, paraganglioma, dermoid cyst. 7. Hydatid cyst—very rare. Multiloculated with nonenhancing septa

Answer 59

1. Germ cell tumours—95% of testicular tumours in young men, nearly always unilateral. Usually hypervascular on US. Risk factors include undescended testes (even if corrected), previous contralateral germ cell tumour or positive family history. The primary tumour may ‘burn out’, regressing into an irregular focus of calcification, but any metastases will remain. (a) Seminoma—~50%. Typically a solid well-defined homogeneously hypoechoic mass contained within the testis. May be multifocal. Necrosis and calcification are rare. 25% have retroperitoneal nodal disease at presentation. αFP and ß-HCG are usually normal. (b) Nonseminomatous germ cell tumour—usually contains a mixture of embryonal, teratoma, yolk sac and choriocarcinoma components. More aggressive than seminoma and more heterogeneous due to necrosis, haemorrhage, cystic change and calcification. Often invades tunica albuginea. αFP, ß-HCG and LDH often raised. Pure yolk sac tumour is the most common testicular tumour in children. (c) Epidermoid cyst—most common benign testicular tumour. Characteristic ‘onion skin’ appearance on US: well-defined avascular mass containing concentric echogenic rings of 296 Aids to Radiological Differential Diagnosis keratin. Alternatively may be hypoechoic with a central echogenic focus (target appearance). May be rim-calcified. 2. Sex cord stromal tumours—usually benign but indistinguishable from malignancy on imaging; usually small, solitary, hypoechoic and hypervascular. Leydig cell tumours are the most common and may secrete testosterone or oestrogen. Sertoli cell tumours can calcify, may secrete oestrogen and are associated with Peutz-Jeghers syndrome and Carney complex. Rarer subtypes include granulosa cell tumour and thecoma-fibroma. 3. Lymphoma*—most common testicular malignancy in men >60 years, usually secondary. Hypoechoic and hypervascular on US, often multifocal and bilateral. May be diffuse. Leukaemia can look identical. 4. Metastases—rare, usually in patients >50 years. May be bilateral. Most common sources include prostate, lung, kidney, colon and melanoma. 5. Cystadenoma of the rete testis—rare. Multiloculated cystic tumour arising from rete testis. Has mass effect and may extend beyond testis (in contrast to tubular ectasia). Indistinguishable from cystadenocarcinoma therefore needs excision. 6. Other rare tumours not limited to the testis—e.g. haemangioma, leiomyoma, lipoma, sarcoma, plasmacytoma, carcinoid tumour, neurofibroma. Apart from lipoma (well-defined and hyperechoic), these do not have specific imaging findings

Answer 60

1. Tubular ectasia of the rete testis—geographic cluster of numerous small cysts replacing the mediastinum testis. No mass effect or Doppler flow. Often bilateral, more common in older men. 2. Simple cyst—2–20 mm; unilocular, anechoic with an imperceptible wall. Usually solitary and often located near the mediastinum. 3. Intratesticular varicocoele (mimic)—serpiginous with venous flow on Doppler

Answer 61

1. Testicular torsion (a) Acute—presentation <24 hours. Enlarged isoechoic (early), hypoechoic or heterogeneous (late) testis ± hydrocoele and epididymal enlargement. Colour Doppler: absent testicular flow (complete torsion) or reduced diastolic arterial flow Adrenals, urinary tract, testes and prostate 297 9 (partial torsion <360 degrees); normal peritesticular flow. A twist in the spermatic cord may be seen (most specific sign). (b) Subacute or missed—presentation at 1–10 days. Hypoechoic heterogeneous testis due to infarction. Colour Doppler: absent testicular flow; increased peritesticular flow. Testis atrophies in the chronic phase. (c) Spontaneous detorsion—colour Doppler: normal or increased testicular flow; increased peritesticular flow. 2. Segmental infarction—due to infection, trauma, transient torsion, vasculitis (most commonly PAN), sickle cell disease or hypercoagulable states. Geographic hypoechoic hypovascular area extending to periphery of testis

Answer 62

1. Epididymoorchitis—generalized testicular and/or epididymal swelling and hypoechogenicity initially; progresses to patchy focal low reflectivity. Hypoechoic areas are hypervascular. Isolated orchitis is rare except in mumps. Complications occur in 50%— abscess, necrosis, haematoma and testicular atrophy/scarring. 2. Abscess—complicating epididymoorchitis, often in diabetics or those with mumps. Hypoechoic (or mixed) with an irregular ill-defined wall and low level internal echoes. No internal vascularity, but peripheral hyperaemia is often seen. 3. Granulomatous infection—e.g. TB, brucellosis, syphilis, schistosomiasis, leprosy and fungal infections. Presentation is usually subacute, and pain is less marked. US appearances vary, ranging from diffuse epididymoorchitis to a focal abscess or mass mimicking malignancy. In TB and schistosomiasis, other sites of urinary tract involvement are usually present. TB may also create a sinus tract to the scrotal skin. Other infections tend to occur in immunocompromised patients

Answer 63

1. Testicular haematoma—hypoechoic and avascular. History of trauma is indicative. 2. Testicular sarcoidosis—typically presents in Afro-Caribbean men (in whom testicular cancer is rare) with multiple bilateral small painless hypoechoic masses in the testes and epididymides. Usually occurs in the presence of multisystem involvement. 3. Testicular lipomatosis—multiple, usually bilateral, small well-defined hyperechoic lesions. No mass effect or hypervascularity. Pathognomonic for Cowden syndrome. 4. Testicular adrenal rests—seen in congenital adrenal hyperplasia. Variable echogenicity; usually multiple, bilateral and located next to mediastinum testis. 5. Other rare disorders not limited to the testis—e.g. malakoplakia, amyloidosis, Rosai-Dorfman disease. Nonspecific testicular mass indistinguishable from malignancy.

Answer 64

1. Epididymitis—acute history of pain. Enlarged, hypoechoic, hypervascular epididymis with a hydrocoele and skin thickening ± involvement of testis (epididymoorchitis). May be complicated by an epididymal abscess: complex cystic lesion with an irregular wall, no internal vascularity with surrounding hyperaemia. Consider granulomatous infection (e.g. TB) if presentation is subacute. 2. Spermatocoele—unilocular or multilocular cyst in epididymal head containing low level echoes (‘falling snow’) representing spermatozoa. 3. Epididymal cyst—unilocular simple cyst in any part of epididymis, no internal echoes. 4. Postvasectomy ectasia—epididymis enlarges and appears heterogeneous due to obstruction and dilatation of epididymal ducts. A sperm granuloma may also be seen. 5. Sarcoidosis*—epididymal enlargement or focal hypoechoic nodules. More common than testicular involvement. Usually bilateral, in the presence of disease elsewhere. 6. Neoplasms—most are benign. (a) Adenomatoid tumour—most common, benign. Well-defined, solid, hypovascular, often hyperechoic on US, most common in the tail. (b) Leiomyoma—well-defined hypoechoic mass ± cystic change, usually in the head. (c) Papillary cystadenoma—benign. Typically a mixed solid-cystic mass in the head. Associated with vHL (especially if bilateral).Adrenals, urinary tract, testes and prostate 299 9 (d) Lymphoma*/leukaemia—rare, often bilateral. Testicular involvement is more common and more extensive (in contrast to sarcoidosis and TB). (e) Metastasis—e.g. from prostate, kidney, GI tract, pancreas. Rare. (f) Other rare tumours—e.g. lymphangioma (multiloculated cystic mass), haemangioma, neurofibroma, sarcoma, adenocarcinoma and plasmacytoma. 7. Epididymal filariasis—parasites can be seen moving within dilated epididymal lymphatics on US (‘filarial dance sign’). Endemic in tropical areas.

Answer 65

1. Hydrocoele—serous fluid collection between layers of tunica vaginalis. Can be congenital (due to patent processus vaginalis) or reactive to scrotal infection, torsion or malignancy. Envelops the testis (cf. large epididymal cysts which displace the testis). 2. Pyocoele/haematocoele—due to infection (pyocoele) or trauma/ surgery (haematocoele). Complex paratesticular fluid collection with internal echoes and septations, ± gas if pyocoele. 3. Tunica albuginea cyst—2–5 mm, unilocular or septated, located on the surface of the testis. 4. Scrotal pearl—see Section 9.40. 5. Fibrous pseudotumour—benign reactive fibrous proliferation, typically arises from tunica vaginalis. Single or multiple hypoechoic hypovascular masses ± calcification ± hydrocoele. 6. Other rare benign tumours of the tunica vaginalis—e.g. adenomatoid tumour, leiomyoma (can also arise from dartos muscle), lipoma, solitary fibrous tumour. 7. Malignancies of peritoneal origin involving the tunica vaginalis—rare. (a) Metastasis—disseminated peritoneal malignancy + a patent processus vaginalis allows spread of tumour (and fluid) into the tunica vaginalis. (b) Mesothelioma—typically in older men with a history of asbestos exposure. Usually presents as multiple masses or nodules on the tunica vaginalis + hydrocoele. Benign variants can also occur in younger men. (c) Ovarian-type epithelial tumours—histologically identical to ovarian surface epithelial tumours and primary peritoneal carcinoma. Usually mixed solid-cystic. 8. Supernumerary testis—isoechoic to, and smaller than, the adjacent normal testis. 9. Splenogonadal fusion—ectopic splenic tissue attached to the testis (nearly always the left; may be undescended). Homogeneously hypoechoic on US, may have a prominent feeding vessel ± a band of splenic/fibrous tissue connecting the testis to the spleen

Answer 66

1. Varicocoele—dilated pampiniform plexus of veins >2 mm on US. Seen in 15% of adult men, usually on the left side. Important to exclude a retroperitoneal mass, particularly in the older patient, if bilateral or if the history is short. 2. Inguinoscrotal hernia—protrudes from the inguinal canal into the scrotum, enlarges with Valsalva. 3. Lipoma—most common extratesticular nonepididymal tumour. May mimic a hernia but is separate from the deep inguinal ring and does not enlarge with Valsalva. Well-defined, avascular, usually uniformly hyperechoic. 4. Hydrocoele of the spermatic cord—may be encysted (resembling a simple cyst) or may communicate with peritoneal space via a patent processus vaginalis (funicular type). 5. Sperm granuloma—occurs following vasectomy at the cut ends of the vas deferens. Well-defined hypoechoic mass. 6. Spermatic cord haematoma—most commonly following inguinal hernia repair but can also occur due to trauma, ruptured varicocoele or anticoagulation. 7. Leiomyoma—usually in the inguinal part of the spermatic cord (in contrast to leiomyosarcoma, which is usually in the scrotal part). 8. Sarcoma—most common spermatic cord malignancy, most often rhabdomyosarcoma (teenagers and children), liposarcoma or leiomyosarcoma (older men). These present as large heterogeneous invasive soft-tissue masses, apart from well-differentiated liposarcomas, which are mostly fatty and well-defined (albeit difficult to characterize on US). 9. Other rare tumours—e.g. adenomatoid tumour, aggressive angiomyxoma, cellular angiofibroma, haemangioma, nerve sheath tumours, paraganglioma, rhabdomyoma, dermoid cyst, lymphoma, plasmacytoma.

Answer 67

1. Trauma—typically short in length, developing weeks or months after the trauma. Straddle injuries cause strictures of the bulbous urethra. High-energy pelvic fractures cause strictures of the membranous urethra. Iatrogenic trauma, e.g. instrumentation and prostatectomy, causes strictures of the bulbomembranous and prostatic urethra respectively. 2. Infection—usually due to chronic or recurrent gonococcal urethritis. Strictures are usually long/multiple and irregular, most commonly in the bulbous urethra, and may be complicated by a periurethral abscess ± perineal or scrotal fistula. Small contrast-filled outpouchings (periurethral glands) strongly suggest infection. Urethral TB is rare but causes strictures of the anterior urethra with multiple perineal and scrotal fistulae (‘watering can’ perineum). 3. Urethral cancer—usually SCC (anterior urethra) or TCC (prostatic urethra), but adenocarcinoma and rarely leiomyosarcoma, melanoma and lymphoma can also occur. Most arise from the bulbomembranous urethra and present as a palpable mass ± urinary obstruction or bleeding. An irregular urethral stricture or change in morphology of a previously benign stricture suggests malignancy. MRI shows a T2 hypointense mass and aids local staging. 4. Secondary urethral malignancy—rare. Bladder TCC can seed to the urethra. Direct invasion of the urethra can occur from prostatic, rectal and scrotal malignancies. Penile metastases (e.g. from prostate, melanoma, colon) can erode into the urethra. 5. Balanitis xerotica obliterans—lichen sclerosus of the penis. Causes meatal stenosis ± strictures of the penile urethra. 6. Congenital stricture—rare, usually presents in childhood. 7. Benign urethral lesions—very rare, present as a filling defect rather than a stricture. Examples include papilloma, leiomyoma, haemangioma, fibroepithelial polyp (congenital, arises from verumontanum), malakoplakia, amyloidosis and condyloma acuminata (due to HPV infection; multiple papillary filling defects in anterior urethra + cutaneous papillomas on the penis)

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