Master Radiology Notes Urology

8/17/2019 Master Radiology Notes Urology

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Urology 1

URORADIOLOGY

Congeni tal Anomalies

Renal dysplasia:The presence of abnormal tissue within the kidney “ cartilage, muscle, primitive nephrons

and cysts ”

Multicystic kidney (see later)

Renal agenesis:

It is failure of the renal development.

- Bitateral agenesis which is incompatible with life.

- Unilateral agenesis: it is due to failure of development of the ureteric bud from

wolffian duct

1) I.V.U single, hypertrophied kidney with normal pelvicalyceal system .

2) U.S confirm the absence of kidney .

3) C.T. left side: the renal fossa is filled by splenic flexure and pancreatic tail.

Rt side; the renal fossa is filled by small gut, liver

4) Cystoscopy, reveals a single ureteric orifice with absence of the homo-lateral half of

trigone "pathognomonic".

N.B. The ipsilateral adrenal gland may be absent .

+/-VATER: V=vascular, A=anorectal atresia , T=trachea , E=oesophageal fistula, R= renal\ radial

Renal hypoplasia: - A small kidney, normal in position with normal renal outline

- Reduced number of calyces but normal

- Hpertrophy of the other kidney

Renal ectopia, malrotation and fusion:

NB: The fetal kidney develops in pelvis by fusion of the ureteric bud with the primitive

nephrogenic tissue. In the pelvis, the renal pelvis lies anterior to the renal tissue, as the

kidney ascends to upper abdomen it rotates so the pelvis comes to lie on its medial surface

Renal ectopia:

Failure of the normal ascent, the kidney remains within pelvis or the lower abdomen and

deriving its blood supply either from iliac vessels or lower abdominal aorta .

- It is frequently associated e malrotation.

- May be intrathoracic kidney.

D.D.: nephroptosis = redundancy in the length of ureter.


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Crossed ectopia = S- shaped kidney.

- Kidney migrates to opposite side, ureteric orifice retaining its normal position in bladder.

- It is low in position, usually malrotated and fused e the lower pole of normal kidney

unilateral fused kidney.

Malrotation:

- Commonest variety is the renal pelvis ant. to renal vess. retains its foetal relationship to

kidney and calyces lies posteriorly to and on either side of pelvis.

- It may lead to obstruction hydronephrosis or infection.

Fusion:

"Hoarse shoe kidney" commonest

- The kidneys are united in majority at their lower poles by a bridge of renal tissue or

fibrous band ,crossing in front of the aorta, spine and I. V. C.

- The kidney are low in position & close to spine with their long axis parallel to spine, we

have more hydronephrosis and incidence of Wilms.

Renal duplication:

1- Complete:

Involves the renal pelvis and the whole length of the ureter.

- Each division of pelvis is drained by its own ureter opening separately into the bladder .

- Ureter draining the upper moiety always open below and medial to ureteric orifice for the

lower moiety { may be ectopic ureter up to 6 ureters drain the kidney}.

2- Incomplete:

Confined to renal pelvis or the ureter but the ureteric divisions unite in the abdomen or

pelvis "yo yo reflux !!". Commonly associated e urinary infection and reflux.

Ureterocele:Congenital cystic dilatation of lower end of ureter

Types: - Simple: when orifice is within the bladder.

- Ectopic: when orifice lies outside bladder lumen (ectopic ureter).

Effect: obstruction and stone formation.

1) I.V.U

- The dilated lower end when filled e contrast media produces a circular area of increased

density within bladder which is surrounded by a radiolucent halo produced by ureterocele

wall cobra head appearance “ ch ch “. - when it is not filled e contrast round filling defect.


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2) CYSTO-URETHROGRAPHY:

With dense contrast media may obscure the simple ureterocele.

ECTOPIC URETER:

- A case in which the ureteric orifice lies outside the bladder lumen.

- In males, the ectopic orifice, commonly opens into the post. urethra but may open into

seminal vesicle , epididymis and rarely rectum.

- In females ,commonly situated in the vestibule but may open into vagina , cx, uterus,

fallopian tube.

- It is usually associated e duplication of whole length of ureter and orifice draining the

upper moiety .

1) I-V-U:

1- Enlarged renal shadow produced by dilated upper renal segment.

2- Lower segment of kidney is displaced downwards and lateraly Drooping flower

appearance.

3- Ureter draining lower renal segment is deformed by dilated ectopic ureter.

4- Bladder base may be elevated by the dilated ureter.

5- Ureterocele of ectopic ureter usually larger than simple ureterocele obst. of ureters &

may prolapse into urethra urethral obstruction.

2) U.S.

may show a dilated upper moiety pelvicalyceal system.

Congeni tal HYDRONEPHROSIS (see pediatric abd.)

Q:CONGENITAL ANOMAL IES?:

1- Renal dysplasia.

2- Renal agenesis.

3- Renal hypoplasia.

4- Renal ectopia, malrotation, fusion.

5- Renal duplication.6- Ureterocele.

7- Congenital hydronephrosis.

8- Multi cystic disease of kidney.

9- Ectopic ureter, congenital mega ureter.

Normal Variants:

Normal renal outline can be interrupted and resembles renal tumour due to:

1) Dromedary hump.2) persistent fetal lobulation.


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3) Hypertrophied columns of Berteini.

4) Regenerating nodule.

N.B = all can be confirmed that they are normal renal tissue by DMSA.

U.B congenital anomalies:

-Bladder extrophy.

-Bladder duplication.

-Urachal anomalies.

-Bladder calculi , trauma {extra or intra peritoneal} , fistula

D D of uret erocele:

1-Cobra head appearance may be rarely produced by transient dilatation& thickeninig of ureteric

wall following retrograde catheterization or impaction of stone at ureteric orifice.

2-Same appearance may be also produced by bladder tumour arising close to & partially obst. the

ureteric orifice.

3-Lateral & downward displacement of kidney may be produced by mass arising from upper pole of

the kidney or supra renal region.

4-Intra vesical filling defect may be mistaken for gas in rectum, bladder tumour or non opaque

stone,ectopic ureterocele, rhabdomyosarcoma.

5-deformity of bladder base produced by ectopic ureterocele may simulate lobulated filling defect

of a rhabdomyosarcoma.

Aberrant renal artery:

-It arises either from 1)Aorta….commonest, cross infront of P. U. J.

2)Renal a. ..near its origin &passes behind or infront of renal pelvis.

-It usually goes to lower pole of kidney.

Importance:

-Compresses P. U. J. …..cong. hydronephrosis.

-If devided during operation……infarction,renal ischaemia, renal hypertention.

Cystic diseases of the kidney:

A- Renal dysplasia: 1-muticystic kidney.

2- multipe cysts e lower u.t obstruction.

B- polycystic diseases: 1- polycystic disease of the young (AR):

a- In new born B) In child hood

2- In adult (AD).

3- Von Hippel-Lindau syndrome.


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C-Cortical cysts: 1- simple cyst. 3- trisomy syndrome (13-18).

2- multi locular cyst. 4- tuberous sclerosis.

D- Medullary cysts :

1-medullary sponge kidney.

2- medullary cystic disease.

3- papillary necrosis. 4)pyelogenic cysts.

E- Miscellaneous Intra renal cysts:

1- Traumatic : hematoma.

2 - Inflammatory: T.B,hydatid.

3- Neoplastic: cystic degeneration of neoplasm.

F- Extra - parenchymal cysts:

1-para pelvic cyst .

2- perinephric cyst “urinoma “.

G-Cystic dialysis disease .

Multicystic kidney:

-Non familial,usualy uni lateral.

-It may be associated e other congenital anomalies e.g.TOF,VSD.

-Pathology:

The entire kidney is composed of numerous cysts, contain clear fluid and are embedded inundifferentiated mesenchymal tissue ,but no identifiable renal tissue.Usually unilateral to be

differentiated from polycystic kid.

-C\P : the commonest cause of abdominal mass in infancy.

-Radiologically:

1-Plain:

- Large mass extending from loin displacing the gass shadow.

-Cyst wall calcification “Ring like densities”.

2- I- V-U:- Mainly reveal non - functioning kidney.

- Draining ureter is absent or atretic.

- Compensatory hypertrophy of other kidney.

3- U / S:

-Multiple non- communicating cysts, variable in size resembling a bunch of graps with no

identifiable renal sinus.

4-C.T

-Replacement of kid. by a large mass containing numerous cysts with septa.-Cyst wall calcification.


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D.D

1- wilm’s tumour 2- congenital hydro nephrosis

Polycystic disease of kidney:

A- poly cystic disease of young :

Rare ,AR, familial, bilateral.

Pathology:

- Cystic(=ectatic) dilatation of tubules of renal cortex and medulla

and periportal fibrosis (usu. bilateral).

- In infantile type renal changes predominate.

- In child hood periportal fibrosis predominates.

- failure of fusion of metanephros with its duct enlarged kid. & its entire parenchyma is replaced

by minute cysts representing dilated tubules& glomeruli.

Infantile polycystic kidney:

Presentation in the first day of life e -greatly enlaged kid. e renal failure.

-enlaged liver.

I.V.U:

-Enlarged kidneys with the characteristic striated mottled nephrogram (streaks radiating

from renal papillae to renal cortex)- Impairment of renal function non visualization of calyces .

U.S:

- huge enlaged kidney(s).

- Increased renal parechymal echogenicity(interfaces by walls of tubules) with loss of the

cortico- medullary differentiation “bright echo pattern” because cysts are so small to be

resolved by U.S.

C.T:

-Bilateral enlarged kidneys with exaggerated foetal lobulation.- On enhancement mottled app. in cortex and medulla representing dilalated

tubules

(streaks in parenchyma)

Childhood polycystic disease:

- Age 3.5 years.

-C/P: symptoms & signs of portal hypertension( same as above)while renal disease is mild.

A) I-V-U:

-Enlarged kidneys with smooth outlines.-Mottled nephrogram in advanced cases .


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B) U S:

-As in infantile type.

-Increase echogenicity of the liver due to periportal fibrosis.

C)C.T:

-Areas of low attenuation representing tubular ectasia .

-Mutiple liver cysts communicating with bile ducts.

-May be splenomegally & ascitis =P+ +

N.B .cysts don’t communicate:

Mul ticystic: dysplasia undiff. Tissue inbet….atretic.

Adult polycystic: A D normal Tissue inbet…..ureter

infantile (small cysts can’t be resolved by US)

Adult polycystic disease :

- familial, AD.

-C/P: - presented after 3rd decade with :-

1- Loin pain . 4- Hypertension.

2- Heamaturia. 5-Manifestations of renal failure.

3- Abdominal mass .

-Pathology: - The renal parenchyma is replaced by numerous cysts with variable amount of normal

renal tissue are interspersed between cysts.

-May be cystic changes in liver , pancreas , spleen.

-Radiologically:

I-V-P:

1- Renal enlargement e lobulated outline.

2- Distortion of pelvicalyceal system , which varies (according to no, size &position of

cysts) “Swiss-cheese”: (a) Early cases only renal enlargement.

(b) Advanced cases elongated deformed major & minor calyces.

SPIDER LEG appearance .

-Minor calyces may be stretched by adjacent cyst elongated crescent .

- Major calyces may be displaced , elongated & narrowed.

- Protrusion of a cyst into renal pelvis deformity of pelvis with filling defect

*Nephrotomography: well defined defects in nephrogram .


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U.S:

1. Renal enlargement.

2. Multiple cysts of varying size which generally don’t communicate with

pelvicalyceal system.

C.T:

1-Renal enlargement.

2- Multiple cysts of varying size, shows water density. Increased density in infection or hge.

3- calcified cyst wall.

Angiography:

shows curvilinear displacement of the arterial branches.

MRI: .

Von-Hippel- lindau syndrome (AD)

- Rare, A.D.

-Has many similarities to adult polycystic disease.

*C-N-S: haemagio blastoma , retinal angioma .

* Renal carcinoma and cysts.

* Tumours and cysts of any other abdominal organs.

Simple renal cyst:

- 50% of population. – commonly >50y.-usually cortical in origin, of variable sizes (few m.m to 25cm).

-C/P:

- Mainly silent.

- Large cyst may present as palpable mass producing symptoms by compression of the

adjacent structures .

- Complications:

hge or infarction within the cyst

-Radiologically:A-Plain U T:

1- A bulge on renal surface , displacing renal shadow.

2- Ring calcification in 30%.

B- I V U:

-The distortion of pelvi -calyceal system depends on size and position of cysts:

1- Peripheral cyst : displace, elongate a single adjacent minor calyx.

2- Central cyst : displace , elongates and seperate adjacent major calyx .

3- Cyst in hilum: - distortion and displacement of renal pelvis & ureter.- Compression of ureter or pelvis Hydronephrosis with a filling defect in pelvis.


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* Nephrotomography:

Sharply defined regular defect .

C) U. S.:

well defined , thin walled anechoic pattern with distal enhancement (posterior

enhancement).

D) C-T:

-Non enhancing (if enhance tumour or abscess) .

- Sharply defined regular lesion e renal parenchyma of low attenution

(0-20 H.U) .

- May show calcification in cyst wall or infection or hge(atten. Value)

E)Angiography:

Avasculasr lesion causing displacement and elongation of the arterial branches .

F)Cyst Puncture (U S or C T guided):

* Aspriation of cyst fliud cytology and injection of water -soluble contrast

media.

N.B.: pyelogenic(calicyeal) cysts:

Type 1 diverticulae: polar in position

communicate e calyceal fornix by narrow isthmus.

Type 2 diverticulae: mid polar

communicates directly e renal pelvis.50% stones .

Cong. or acquried d.t ruptured abscess or adjacent cyst.

MEDULLARY SPONGE KIDNEY:

-Cong. disease in which renal medulla is replaced by a number of small cysts “sponge

like appearance.”

- In 80% calculi result from retension & precepitation.-The renal cortex & pelvis are normal .

-C/P: symptoms of complications as secondary infection & passage of stones.

-Radiologically:

A) Plain

- Calculi vary in no, small, very dense, and occur in groups bunch of grapes.

B) IVU

* Large kid.( with medullary calcification).

* Majority of cysts fill with contrast , round, smooth & vary in size.


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- A linear slightly irregular channles , radiating into medulla produced by dilated tubules

(communicate e pelvi calyceal system).

- Enlarged minor calyx draining affected segment forming a wide arc.

C- U/S

- well defined, highly echogenic pyramides d.t multiple cysts(not parenchymatous as

young polycyst.)which is too small to be resolved by echo.

D- C-T

-Enhanced scan shows small medullary cysts & dilated tubules.

Medullary cystic disease (Juvenille nephronophthis)

- Rare.

- Present in childhood with renal failure.

-Radiologically :

A) High dose nephrotomography lucencies in medulla .

B) U S widening of central echogenic area.

C)C-T small cysts demonstrated at cortico -medullary junction.

Para -pelvic cycts :

-Lies in hilum of kidney outside renal substance which are believed to be result of lymphatic

obstruction .A) I-V-U:

Soft tissue mass may distorte the renal pelvis and may causes obstruction and

hydronephrosis.

B)U-S:

Well defined thin walled cystic structure in the renal hilum.

C)C-T:

Thin walled low attenuation (H2O density) cyst in the renal hilus surrounded by a halo( by

renal sinus fat).D-D Renal sinus lipomatosis .

Peri- nephric cyst (urinoma):

-Collection of a clear fluid within the renal capsule surrounding the kidney results from

extravasation of urine secondary to acute urinary obstruction or trauma.

A) I-V-U: Enlargement of renal outline.

B)U S & C T: Encapsulated fluid collection surrounding the kidney.

C)Isotope: differentiate urinoma from other causes of collection by gradualuptake inthe collection.


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Renal Neoplasms:

A) parenchymal r enal tumous:

1- Benign tumours:

-Angiomyoloma .-Oncocytoma ( small solid mass, hypodense)

- Reninomas ( isodense hypovascular subcapsular)

- Multi locular cystic nephromas.

- Meso balstic nephroma.

- Mesenchymal tumours ( Fibroma, myoma , Lipoma, haemangioma)

2- Malignant tumours :-

Primary - Adeno carcinoma (hypernephroma)

-Nephro blastoma (wilms tumour )

- Sarcoma

- Lymphoma (V. rare )

Secondary- metastesis

B- Tumours of the renal pelvis and ureter(= urothelial tumours):

1)Epithelial origin commonly Malignant

- transitional cell carcinoma ..... papilliform

- squamous cell carcinoma ...... ulcerated plaque & stricture

2) Non epithelial origin commonly benign

- haemangioma , fibroma , myoma

3)Cholesteatoma:-

It is not a true tumour( it is a filling defect formed by desquamated stratified squamous epith

which result from squamous metaplasia of transitional eqith d.t chronic irritation e.g stone )

STAGING( CT):

T 1confined to capsule +mild calyceal displacement

T 2 lange T. confined to capsule+ calyceal or pelvic displacement

T3 A perinephric or peripelvic fat

B thrombus in Renal vein

C thrombus in I-V-C

T4 surroundings & may be distal metastasis

ORIGIN:

- arises from ! epith cells of renal tubules, it may develop following cortical adenoma

PATHOLOGY:

Age: above 40 years, more in males.Morbid anatomy: - rounded mass in the upper or lower pole.

- surrounded by stretched capsule.


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- on section it shows yellow colour d.t cells containing lipids & cholesterol.

- shows areas of hge and necrosis .

- it infiltrates capsule late.

Microscopically: - large rounded malignant cells arranged in cords & solid masses.

- cells may be large highly vaculated or small e dark granular cytoplasm

- scanty and vascular stroma.

- many areas of hge and necrosis

Spread : - local.

-Bloodcannon ball metastases(more common)

-Lymphatic

Malignant renal cell carcinomaAdenocarcinoma (hypernephroma):

-Incidence: 1) age > 40 years 2) sex : 3:1(M:F)

3) 80% of the renal tumours .

4) usually unilateral (Bilateral tumour (4%)occur in poly cystic kid.& Von-hipel-

lindau syndrome and pts in chronic haemodialysis.)

-C/P:

- Cardinal manifestation: Loin pain,painless ,early haematuria,& palpable mass.- Metastatic manifestation: deposits in lung, brain or bone …symptoms.

- Associated features: polycythemia, anaemia ,hypercalcaemia hypertention, unexplained

fever, malaise&w.t loss ( = para malignant syndrome)

-Imaging:

A) Plain U.T.:

-Soft tissue mass bulges from renal outline.

-Calcification (diffuse or amorphous may be seen in 6%).

B) I.V.U:-Nephrogram : bulge in renal outline or diffuse renal enlargement.

-Nephro- tomography :

shows irregular filling defect in the renal parenchyma of patchy density.

Pelvi-calyceal:either

1)Compression of pelvis and calyces displacement , elongation , attenuation

and distortion (DEAD!!)

2) extension of the tumour into :

* Renal pelvis filling defect.* Calyx its amputation or filling defect .


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* Renal vien its obstruction diffuse renal enlargement + renal non-function.

C)U/S:

-Solid renal mass which usually has irregular margin& distortes renal outline.

- May be highly echogenic or isoechoic (diagnosed by its mass effect).

- May shows foci of dense echoes due to calcification or areas of low echogenicity due to

necrosis or hge .

- Renal vein or I-V-C involvement can be demonstrated.

Stages of renal cell carcinoma :

Stage I Tumour confined to renal capsule.

Stage 2 Tumour breaks capsule into perirenal fat (Gerotas cap. Intact).

Stage3 Vascular invasion or regional LN spread.

Stage4 Gerotas fascia invaded or distant metastases.

D) C/T:

the method of choice for pre operative staging:

1-Soft tissue mass:

*on precontrast scans:

hypodense mass distort renal outline and shows areas of breaking down or calcification.

* on post -contrast scans :

- vascular tumors

a transient period of marked enhancement during arterial phaseof rapid I.V bolus injection . Subsequently the tumour enhances to a degree less than renal

tissue patchy app .

-Avascular tumour no enhancement.

2-Extension of tumour through renal capsule:

nodular infilterates of soft tissue density within the lucent perirenal fat .

3- Renal vein involvement :

-best demonstrated by rapid sequence scanes at level of the renal vein

following bolus injection-the presence of low atten. area within lumen of an opacified vein

(=definit diagnosis)

-other signs of venous occlusive lesions:

-Diffuse renal swelling.

- Prolongation of cortical opacification time.

- Dilatation of the renal vein .

4-I -V-C affection :

with bolus injection may show dense peripheral ring e less opacified central column


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5-lymph nodal i nvolvement :

enlargement of renal hilar, peri caval, para aortic, retro -crural LN

6- C-T guided biopsy .

7- Distant metastasis.

E)Angiography & phlebography venous lakes

* vascular tumour 1- irregular , beaded pathological vessels( = size and irregular pools of

contrast within tumour =tumour blust

2-A.V shunt may occur

3-Dilated collateral veins suggest renalvein occlusion

4-may show avascular areas of tumour necrosis

*Rarely avascular

* pre -operative renal artery embolization(surgery must be done within 2 weeks before

embolization has to be repeated) or therapeutic (e.g.absolute alcohol or chemo

embolization….cyanoacryl,histoacryl,gel foam.)

F)M R I & ISOTOPE.

Nephroblastoma”Wilm’s tumour”

(adenosarcoma =embryoma)

- Peak incidence 1-5 yrs ( it can occur in young adults)

-Common presentation

abd mass and hypertention(vascular invasion,renin,compression)also pain& metastases

*It arises from embryonic mesodermal remenants from which kidney arises (totipotent cells).

*Before age of 5 yrs.

*It is ! commonest renal tumour of childhood .

*Rapidly growing tumour which destroys ! kid. tissue .

*It infilt. the capsule v. early and extends to the near by structures.

*On section ,cut surfase is homogenous, greyish.

*Shows areas of hge &necrosisMICROSCOPE:

* It is mixed embryonal malig. tumor solid masses of malig epith cells showing glandular or

tubular formatiom +sarcomatous element.

*fusiform or rounded cells.

*smooth or striated muscle, cartilage, myxomatus tissue may be present.

spread :local

Blood

metastases

Radiologically:


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1)plain & IVU:

-Large soft tissue mass displacing bowel loops & may be calcified.

-Distortion of the renal outline & calyces on I-V-P.

-In 10% Non functioning kidney.

2) U-S:

-Moderately echogenic solid mass, may shows areas of low echogenicity due to necrosis +

compressed renal tissue around the mass + renal vein or IVC invasion or comression.

{ DD: with hydronephrosis, Polycystic,multicystic,neuroblastoma}

3)C T:

-Mixed atten. mass e densely enhancing pseudo-capsule produced by compression of

adjacent renal tissue .

- Calcification in 30%.

- Extra-renal extension , venous involvement, nodal involvement,as in adenocarcinoma.

{DD: from other infantile abd mass see ped. Abdomen}

LYMPHOMA:

-It is very rare,common in non - hodgkin, primary lymphoma is very rare.

-The only one e hypoechoic low attenuation!!.

1-plain&IVP:- Diffuse renal lymphomatous infilteration renal enlargement(comm. Bilateral) e normal

outline and elongated attenuated calyces .

{D-D: leukaemia ,multiple myelomas}

2-U.S:

-Shows lymphomatous deposits as well defined hypoechoic e distal enhancement + lymph

nodes+ renal enlargement.

3- C-T:

- lymph deposits appear as low attenuation which don’t enhance. ( Direct extension of retroperitoneal lymphomatous diseaseureteric obstruction, renal

vascular occlusion)

Renal metastasis:

1) C.T indistingiushed from 1ry renal carcinoma.

2) Angio usually avascular.


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Angio-myo- lipomas:

-They are actually hamartomas, consisting of a mixture of muscles ,fat, and blood vessels

(C T density).

-Occur in 80 % of patients e tuberculosis.

-Imaging:

1- I-V-P:

space occupying lesion e a radiolucent component.

2-U-S:

highly echogenic mass.

3- C T:

large mass e fat attenuation value ( 0-(- 60) H-U ) intermixed é areas of increased tissue

density (muscle& blood.vs ).

4-Angio:

highly vascular mass supplied by wide tortous vessles arising from renal arteries e ccc

aneurysmal dilatation,&early venous filling.

5-M R I:

--bright on T1,very low on fat suppresion.

Oncocytoma:

- Rare ,considered to be a low grade hypernephroma.-Common in old age& in males.

-Imaging:

1-IVU& US: usually well defined solid mass.

2- C.T: hypodense well defined mass.

3- Angio: - well defined mass e lucent rim.

-it contains radiating vs in( = spoke wheel pattern)

Muli-locular cystic nephroma:- Common in childhood, considered to be a benign form of wilm’ s tumour.

- Pathlogy:

- Well-encapsulated tumour, contaning multiple cysts of varing size and separated by

thick fibrous septa.

-It may contain foci of malignant cells.

- Cortical adenoma : can be multipte, < 3= benign.

US hyperechoic

CT homogenous

N.B.Hypodense….hypernephroma(oncocytoma low grade varient).


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Lymphoma (only one hypoechoic).

-Fat attenuation…..Angiomyloma.

-Mixed denseties…..Wilm’s(multilocular cystic nephroma…varient benign form).

(mesoblastic nephroma…..cong Wilm’s).

-Lymphoma the only one hypoechoic ,rest are hyper or iso.

-All are hypodense esp.angiomyeloma .Wilm’s is only one mixed.

-All increased vascularity exept reninoma(no CT contrast).

Imaging:

1- plain : soft tissue mass displacing bowel& cacification.

2- I-V-U: intrarenal mass which may herniate into the renal pelvisfilling defect in

nephrogram &displacement or compression of calyces.

3-US: multiple cysts e highly echogenic septa.

4-C T: multiple cysts separated by thick septa which may show enhancement.

5- Angio: avascular mass.

Mesoblastic Nephroma:

-Considered to be congenital wilm’s tumuor.

1- plain: large soft tissue mass.

2- I-V-U: large intra renal mass which displases&distores pelvicalyceal sys.

3- U S:

echogenic mass e cystic degeneration.4- Angio: neo- vasculairty within the mass.

Juxta glomerular tumours” Reninomas”:

- Very rare, renin producing tumour, in young adults.

- Hypertention&increased renin level.

- Uusually solitary, small (3cm) located under renal capsule” subcapsular.”

1) I-V-U: small mass lesion within kidney.

2) US: well defined hyperechoic mass.3) C-T: isodense mass ,doesn’t enhance.

4) angio: hypo vascular, small, subcapsular mass .

Pseudo tumors of the kidney:

-Anatomical aggregates of normally-functioning renal tissue which resemble pathological

mass e.g:

1- Dromedary hump: Bulging of normal left renal outline(mid-portion), inter-papillary line

runs parallel to the renal outline.2- Splenic impression “hump”: an apparent bulge inferiorly.


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3- localised hypertrophy: adjacent to an area of pyelonephritic scarring.

4-Hilar lip: hyperplasia of parenchyma adjacent to renal hilum.

5-Renal sinus fibro-lipomatosis: ---proliferation of fat within the renal sinus ,frequently

occur in response to atrophy of renal substance.

6- porominent column of Bartin: ---invagination of normal cortical tissue.

--- the added cortical thickness localised mass

displacing the adjacent calyces.

* C.T: a nodule has the same att. value of renal parenchyma.

* Angio: displacment of interlobular arteries e normal arcuate arteries entering the mass.

7- congenital hypertrophy of renal papilla:

* I-V-U: filling defect, continous e papilla& protruding into calyx.

* C.T: the same att. Value of normal renal parenchyma.

8-Persistant foetal lobulation.

N.B.:.Staging of ureteric tumours:

A: mucosa only.

B: superficial muscle layer.

C: penetrating the wall.

D: periureteric structures.

Urothelial Tumours:C/P: loin pain and haematuria.

Imaging:

1-I-V-U:

a) Papillary tumours( = Transitional Cell Carcinoma or Papilloma): 90%

-Filling defect e lobulated surface.

-The ureter dilates at the site of tumour to accomodate tumour expanding lesion.

-Retrograde urography:

* Protrusion of tumour into the dilated ureteral lumen wine glass appearance.*Trapping of contrast within interstices of papillary growth stippled appearance.....

“stippling sign.”

B) Sq. Cell carcinoma : 10%

- Usually manifests itself as a stricture without filling defect.

- In renal pelvis usually causes strictures obstruction and infiltration of perirenal tissue.

2- U/S:

iso echoic solid mass has an echogenic rim due to renal sinus fat.-shows -presence of hydro nephrosis


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Urology 19

3-C.T:

1- mass within renal pelvis e slight enhacement mass may lead to balloning of renal pelvis

obstruction of the calyces with proximal dilatation.

-Extension to wall of renal pelvis,renal sinus fat, renal parenchyma and perirenal spaces

can be shown.

2- ureteric tumors: irregular thickening of ureteral wall e invasion of retroperitoneal fat

and obst. Uropathy.

4-Angio: relatively avascular.

N.B.: ureteric inflammation & infections:

1- ureteric tuberculosis.

2- schistosomiasis.

3- leucoplakia (sq. metaplasia d.t. chronic infection).

4-uretrites cystica.

N.B .: medially placed ureter:

1-Retroperitoneal fibrosis.

2-pelvic lipomatosis.

3-ureterolysis.

N.B .: ureteric strictures:

*cong.* traumatic :surgery.

* inflammatory / Infective : TB,Bilharziasis.

* radiation.

*Malig ( primary or direct spread from retroperitoneal tumors).

D-D A) of fi ll ing defect:

1-Benign ureteric tumours (fibroepthileal polyp).

2-Blood clot in renal pelvis.3-Non- radioopaque calculi.

4- Sequestrated papilla.

5- Schistosomiasis .

6-T.B. granulation tissue .

7-Rarely fungal ball .

8-Air bubble, cyst, papilloma ,cholesteatoma.

B) of stri cture :

1-T.B. 2-Bilharziasis.3-Sq. cell carcinoma. 4- Ureteric involvement by retroperitoneal disease.


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Urology 20

D.D RENAL MASS:

A)cystic -( cystic disease of kidney) B)Solid

1-renal dysplasia. 1- Benign.

2-polycystic. 2- Malignant.

3-cortical.

4- medullary. 3- Pseudo Tumour.

5-miscellenous. 4- inflammatory masses:

6-Exraparenchymal. * Renal abscess.

* tuberculoma.

* xanthogranuloma,pyelonephritis.

Investigations:

-clinically suspected renal mass:

* plain and I V U+/- tomography.

* US:

(simple cyst or solid or Mixed)

*C.T or angio . *aspiration cytology.

*C T or angio.

1-Plain:a.UTI. Soft tissue mass, displacing gas shadow.

ii. Calcification curvilinear in simple cyst.

punctate or amorphous tumour.

calcified tuberculoma.

iii. Metastatic deposits in pelvis and spine.

iv. inflammatory abscess loss of psoas line.

scoliosis : concave to side involved.

b. Chest :-T.B.

-Cannon ball metastasis.

2-I.V.U.

3-U/S.

4- C.T.

5- Angio.

6- Isotopes non specific area of activity :

a. Cyst. b. Inflammatory mass.c. Neoplasm.


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Urology 21

Tumours of the bladder:

A. Primary tumour :

a. Epithelial :

I. Papillary papilloma

papillary carcinoma

ii. Non papilla transitional cell carcinoma

epidermoid carcinoma

adeno carcinoma

b- Connective tissue :

i. Haemangioma.

ii. Neurogenic tumour.

iii. Sarcoma.

B. Secondary tumour :

Rare, usually seedling from pelvis of the kidney, ureter or extension from surrounding.

-TNM Staging of UB tumours :

Tis……. pre invasive & in situ.

T1…….doesn’t invade beyond : lamina propria.

T2…….Invades superf. ms layer.

T3……. A- Deep ms layer.B- Extends through bladder wall.

T4……. A- prostate, uterus or vagina.

B- pelvic side walls + abd. Wall.

No……No regional LN metastases.

N1……Single ipsilat. ext. or int. iliac LN.

N2……Contra lat., bilat., or multiple LN.

N3……Fixed regional LN.

N4……Juxta regional LN (common iliac, aortic, inguinal). Mo……No distant metastases.

M1……Distant metastases.

N.B.) MRI:

- Can detect tumours > 1 cm diameter (appropriate RF pulse).

- Tumours of UB dome or base sagital & coronal images while those of lat walls coronal &

transverse images.

- On T1 weighted medium signal intensity (> fat & urine).

- Advantage : detects intravesical part & perivesical fat extension also pelvic LN detection without


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Urology 22

need for DTPA gadolinum + fat suppression technique.

- On T2 weighted varying degrees of high signal intensity ?? paramagnetic effect (fig. 41.37).

Carcinoma of bladder :

-It is commonest carcinoma in Egyptian males.

-Pre-cancerous lesions :

1. Bilharziasis.

2. Exposure to aniline derivatives.

3. Abuse of analgesic.

4. Smoking.

- Pathology:

Non Bilharzial Bilharzial

1. Age > 60y

2. Site : trigone

3. Macrocop. papillary

nodular

ulcerative

4. Microscopic : transitional cell

20-30y

lateral side then spread

-Nodular fungating mass

-malig ulcer

-diffuse infilteration

sq. cell. carcinoma.

-Imaging :

Diagnosis is usually established by cystoscopy. Then staging by:A. Plain ::

-Presence of calcification in trans. cell carcinoma.

B. Cystogram :

- Papillary tum. well defined lobulated filling defect.

- Non papill. tum plaque like irregular defect with ill defined margins.

- Reflux can occur, when there is ureteric involvement.

C. U/S:

- Trans abdominal, trans urethral, trans-rectal.-Can demonstrate tumours as small as 5mm in diam. and the extent of bladder wall

invasion.

D. C/T:

Best done with filling of small bowel.

rectum & sigmoid by enema.

They not diff between T1 & T2.

-MRI can diff. T2 & T3A.

-Due to presence of peri-vesical and pelvic fat, extra vesical extension can be easily detected by C.T.


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Urology 23

-Lymph node involvement ext., internal and common iliac glands.

E. Lympho-graphy: to detect lymph. nodes.

Vesical diverticula :

-Causes :

1-congenital.

2-due to lower U.T obstruction BNO.

prostate.

ureth.

3-traction(sliding hernia,adhesions).

4-false

-Ef fect :

- Urine stasis infection & stone formation.

- Reflux if ureteric orifice lie inside diverticula.

- Obstruction of lower ureter by a large diverticula.

-M icturating cystogram :

- Should be done, as simple cytogram is an unreliable.

- The divert. may be quite small on the resting film, but become greatly distended during

micturation.

-plain : stone not changing position.-DD :

1. Vesical duplication.

2. Hour glass bladder.

(They contract normally and empty during micturation.).

Neurogenic bladder :

-Loss of normal control of micturation due to lesion of spinal cord (chordoma is commonest

cause) and peripheral nerves. Radiolog. app.:

A).U.M.N.L “micturating cystogram”:

1. A large atonic, smooth walled bladder.

2. Enlarged residue.

3. Complete absence of bladder contraction.

4. Voiding produced by abdominal compression.

5. Bladder neck and urethera are normal.

B) L.M.N.L “micturating cystogram”: 1. Reduced capacity of bladder.


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Urology 24

2. Wall is thick and trabeculated.

3. Sacculation “pin tree” shape.(christmas tree).

4. Bladder neck is narrowed by hypertrophied bladder wall.

+/- vesico-ureteric reflux is a common association.

Congenital anomalies:

1-Ectopia vesica : -ass e diastasis of symph. Pubis(plain,IVP,US for obst).

-increased incedence of adenocarcinoma.

- ttt: ureter diversion surgery.

2-Duplication : each pair has a ureter+urethra. 3-Urachal anomalies.

Bladder trauma :

-Causes : -Fracture pelvis.

-Instrumentation.

-Penetrating wound

-Imaging :

a. Plain :

-Fracture pelvis.

-Obliteration of psoas outlines in extra peritoneal rupture.

-In penetrating wounds

air fluid level. b. I.V.U :unriglity of upper U.T.

may shows, extra-vasated urine.

c.cysto-gram: -may shows deformity & displacement of bladder by pelvic haematoma.

-Intra-peritoneal extra-vasation contrast. medium gravitates to most

dependent part of pelvic cavity and loops of gut produce a ch. ch. round filling defects.

- Extraperitoneal contrast media go to perivesical spaces.

Stones :

Ca phosphate single, large, laminated

Renal calcification:

1. Renal calculi. 2. Nephro-calcinosis.

3. Dystrophic calcification.

1. Renal calculi:

- Most commonly seen in middle age.-Etiology of stone formation :


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Urology 25

1. Stasis : due to cong. or acquired structural abnormalities :

1. Horse shoe kidney.

2. Vesical divert.

3- Med. sponge kid.

4- P.U.J obstruction.

5 - Lower U.T obst.

6- Papillary necrosis ... necrotic tissue forms a nidus for stone formation.

7- Ch. u.t. infection with urea splitting organism e.g. proteus.

2. Metabolic disorders :

a. Ca. stones : hyper-calcaemia hyperparathyriodism.

Idiopathic.

b. Cystine stones : in cystinuria (familial disease in which there is failure of normal tubular

absorption of amino acid).

c. Uric acid calculi : disordered purine metabolism as in gout.

d. Xanthine stones : failure of normal oxidation of purines.

e. Oxalate stones : 1ry hyperoxaluria.

2ry (enteric)due to disturbance in bile acid metabolism as in Crohn’s,

dis.&ulcerative colitis.

-Pathology :

-The great majority of stones are radio-opaque( 80%) consisting of a fibrous matrixcovered by crystals.

a. Ca-oxalate stone : laminated & have “a nodular mulberry app.”

b. Phosphate stone : often attain a great size and may form cast of the renal pelvis & calyces

stag horn st..”

c. Ca carbonate stone milk of Ca.

-DD of Radio opaque stones :

1. Region of kidney : gall stones, calcified costal cartilage and mesentric glands.

2. ureter tips of trans. processes.3. U.B calcified iliac vs, phleboliths & fibroids.

d. cystine stones : less radio-opaque ch. ch. milky opacity.

e. Pure uric acid & xanthine stones radiolucent.

-Imaging :

A). Plain shows radio-opaque calculi which may :

- Urinary in origin.

- Or extra-urinary : don’t maintain a constant relationship to urinary

tract in inspiratory & expirat. Films.B).I.V.U :value :


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Urology 26

1. Rodiolucent stones appear as filling defect.

2. To show presence of obst. Uropathy:

urographic finding of acute obstruction : see later.

Urographic finding in chronic obst. see later.

C.) U/S : value:

1. Echogenic foci with post. shadowing stone.

2. pelvi calyceal dilatation.

3. Post-obstructive parenchymal atrophy.

D.) C.T :

- Radoiolucent stone : appear as a high atten. value within the low atten. value of pelvic

calyces “ Pre. Contrast”.

- Differentiate between radiolucent stones and other causes of filling defect ... (give soft

tissue att. value).

2. Nephrocalcinosis (Parenchymal calcification):

-It may be : a.Medullary. b.Cortical. c.Dystrophic.

a. Medull ary nephro-calcinosis:

1. Hyper-parathyroidism hypercalcaemia.

2. Renal tubular acidosis hypercalcemia.

- It is “commonest cause of nephrocalcinosis in children. - Mainly associated with rickets or osteo-malacia.

3. Medullary sponge kidney (struct. abnormality).

4. Renal papillary necrosis (struct changes) calification of necrotic papillae.

5. Oxalosis or hyper-oxaluria : due to high excretion of oxalic acid deposition of ca.

oxalate crystals in “renal tubules”.

6. Other causes of hypercalcaemia :

a. Idiopathic.

b. Hyper vitaminosis D.c. Multiple myeloma.

d. Sarcoidosis. e.Prolonged recumpancy.

B. Corti cal nephro-calcinosis:

1. Acute cortical necrosis usually occurs as a result of Hge in late pregnancy.

- Calcification may take form of double parallel lines :” trame line calcif. “

2. Chronic glomerulo-nephritis very rare.

3. Chronic transplant rejection.


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Urology 27

C. Dystrophic calcif ication due to locali sed disease:

-Usually affect part of one kidney.

1. Infection :- T.B : variable app. of nodular, curvilinear or amorph. calcification.

- Hydatid : curvilnear calcification in cyst wall.

- Abscess.

2. Carcinoma: may be amorphous, irregular or curvilinear.

3.Aneurysm of renal artery curvilinear.

N.B. Non obstr. Dilatation 1)VU reflux

2)pregnancy

3)primary mega ureter

Urinary obstruction:

- Hydronephrosis :

-Dilatation of renal pelvis and calyces + thinning of the renal parenchyma.

NB. : hydro-calicosis:

-dilatation of one or more calyces in the absence of renal pelvis dilatation.

-Usually occurs 2ry to obst. of a calyceal. infandibulum by T.B scarring, calculi, crossed

vessels.

NB. Hydro-ureter :

- dilatation of ureter which either obstructive or non obstructive” v.u reflux.”Causes :

a. Pelvi-ureteric obstruction :

1. Intra-luminal lesions :

- congenital : P.U.J obstruction

Ureteric atresia.

- Acquired stones, blood clot.

Paplillary tumour

fungal ball, cholesteatoma (rare).2. Extra-luminal :

* Intra-mural strictures of ureter : either: - Benign : T.B , Bilharzial, post operative.

- Malignant . Sq. cell carcinoma.

*Extra-ureteric - extrinsic strictures : -Pelvic inflammatory disease

-Retro-peritoneal fibrosis post. operative.

pancreatitis.

-Invasion by tumour e.g. cancer ovary, rectum.

- Crohn’s disease, aberrant renal As.


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Urology 28

b. Infra-vesical obstructive ... “obstructive uropathy:

=Lower UT obst BNO

prostate

ureth. (see later)

- Grading of H.N.:

1. Grade I : Minimal dilatation, characterised by slight rounding or blunting of the calyceal

fornices.

2. Grade II :

- Complete blunting of calyceal fornices

- More calyceal dilatation.

- Shadow of papillae are still easily seen.

3. Grade III :

-Rounding of calcyces with obliteration of shadow of the papillae.

4. Grade IV :

- Extreme calyceal ballooning

(N.B………. Parenchymal thinning is often obvious with grade III, IV).

-Diagnosis :

A).I.V.U:

1. Acute obstruction : commonest cause is impacted ureteric stone.

-I.V.P findings:

Acute obst. Chronic obst.

-Increasingly dense nephrogram

-Modest renal enlargement

-delayed calyceal

opacification(pyelogram)

-dilated pelvis & ureter (up to obst)-pyelosinus extravasation

-Renal size or

-Faint nephrogram no pesistant

nephrogram

-Parenchymal thickness

-Massive hydronephrosis(+dilated tortousureters&poor pyelogram acc.to renal func

-Calyceal crecents.

Late(in both): non functioning kid.

1)Increasingly dense nephrogram( obst. Nephrogram):

- This is the most impressive urographic abnormalites.

- The immediate post-injection nephrogram may be normal or slightly reduced than normal

in density ... The density increases with time to reach peak nephrogenic density 3-6 hrs. ...subsequently fades 24-48 hrs. after contrast injection.


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Urology 29

-It may shows, fine, white lines arranged radially in parenchyma perpendicular to renal

margin ... represent contrast med. within the engorged tubules.

ii) Modest renal enlargement in 50%:

due to enlarg. of renal tubules and interstitial oedema.

iii)Delayed calyceal opacification :

-abscence of contrast medium in collecting system 15 minutes after infection (delayed

films).

- Once opacification occurs it points to site of obstruction and opacification will persist

for hours.

iv) Little dilatation of pelvic calyces & ureter proximal to obst.

v) Pyelosinus extra vasation :(spontaneous)

- Overdistension of the collecting system may causes rupture at its weakest point “calyceal

fornix” extra-vasation of C.M. into the peri-calyceal and peri-pelvic spaces and enter into

the renal sinus.

-Sometimes the extra-vasated urine is encysted urinoma within renal sinus.

2. Chronic obstruction :

A. Renal size : determined by duration & degree of obst. The kidney may be small or large.

B. Absence of obstruct. nephrogram the nephrographic density is characteristically faint

due to obst. atrophy.C. Massive hydro nephrosis.

D. Parenchymal thickness :

- Measured by distance between edge of calyces and the outer surface of nephrogram.

- Normally it ranges from 2.5 cm in mid portion to 3.5 cm at the poles.

- End-stage obst. atrophy is characterised by marked thinning of the renal parenchyma

thin band surrounding the dilated calyces, forming “rim or shell” nephrogram.

E. Calyceal crescents :

- Thin semi-lunar collection of C.M, denser than nephrogram, in the renal medulla, parallelto convex margin of the ballooned calyces.

- They represent, the C.M. within collecting tubules.

B) U/S: -Detection of hydronephrosis in ch. obst.

C) C.T:

Plays a minor role in 1ry diagnosis of obst. than I.V.U & U/S.

D) angiography : not used.

E )Radio istope scans.


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Urology 30

** Antegrade pyelography to determine level & cause of obstruction.

urine sample & renal pelvic pressure .

to opacify collecting system prior to nephrostomy

**When to do nephrostomy pyonephrosis with obst.

severe loin pain.

to preserve renal funtion.

Obstructive uropathy “lower U.T obst”:.

Causes : obstruction at or below the bladder neck:

1. Bladder : bladder neck obst.

2. Prostate : prost. enlargement.

3. Ureter : Ectopic ureter.

4. Urethra : urethral valve obst.

urethral stricture.

urethral diverticula, calculi, tumours.

5. Penis meatal stenosis.

polyp of verumontomus.

-prune belly syndrome Bilat : hydronephrosis

ureth. obst.

undescended testicle

Radiological Signs :

1. General :

A. Signs at upper U.T :

1. Dilatation and increased tortuosity of ureters:

- Early stages confined to one side.

- Late stages biltareal but not necessarily equally.

2. Dilated renal pelvis : uniform calyceal dilat with renal substance.3. Progressive impairement of renal functions.

B. Signs at the lower U.T:

Urethral stricture :

1. Urethral dilatation.

2. Bladder. neck hypertrophy.

3. Vesico ureteric reflux.

4. Trabeculations.

5. Bladder diverticulae6. Vesical residue.


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Urology 31

2.Individual pictures:

A. Bladder neck obst.

Pathogenesis :

hypertrophy of bladder neck as part of the generalised hypertrophy of detrusor muscle

which may be :

1. Primary :

hypertrophy of musculosa.

fibrosis of subserosa

spasm fo neuro muscular incoordination

ii. Secondary due to urethral obst.

iii. congenital very rare.

I ncidence & C/P :

- Adult more common, presented by C/O & O/E of prost. enlargment “prost. is normal”.

- Childhood less common, presentes by retention, R. failure.

Radiolog. “cysto-urethrogram :

1. Trabeculation, saculation and divert. formation.

2. Narrowing of bladder neck.

3. Hypertrophied B. neck protrusion into bladder base intra-vesical impression.

4. Narrowing of distal urethral lumen due to poor flow through the obstructing bladder neck.

5. Vesico-ureteric reflux.DD :

1. Neurogenic disorders : associated with other neurolog. signs.

2. Prominance of bl. neck :. normally, no signs of obst.

3. Spinning top urethra : a + b + c.

basal sacculation (c)

hypertrophied bladder neck (a)

Spinning top urethra.

distal urethral stenosis (b).

B. Prostatic enlargement

- The commonest cause of lower UT obst. in elderly.

- It is due to benign hyperplasia.

prost-carcinoma.

N.B. *433.8cm (2=calculated weight).

*average wt 20gm.

*benign hypertrophy periurethral central zone.


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Urology 32

1. Benign hyperplasia:

Site: transitronal zone (bet.periph. & central zone).

Radiological app.:

1. Plain increased bladder shadow d.t. residual urine.

prost. Calculi.

2. I.V.U.: a. Obst. changes in upper U.T.

b. Enlargement and elevation of lower ureters fish hook app.

c. Elevation of bladder base above sym.pubis

d. Thick wall e trabeculations & diverticuae.

e. Protrusion of prost. into bladder base large, smooth, rounded or lobulated

filling defect…..ccc

f. Residue is present at post evacuat films.

3. Micturating cysto-gram.:

a. Prost. urethra length > 3cm. b.Residual urine.

stretched on surface of gland “slit lumen.”

normal curvature.

deviation with asymmetrical enlargement.

prost. nodule protruding into lumen of the urethra filling defect.

4. Trans rectal U/S : dimensions & volume.

- Diffuse enlargement of gland with an intact capsule.- Homogenous echo pattern, may appear heterogenous if complicated by areas of infection

or stone formation.

5. C.T + MRI:

Homogenous enlargement of gland with well defined border and preservation of fat planes.

Staging:*T1….intracapsular e normal glandular outline

*T2….intracapsular e irregular glandular outline

*T3….carcinoma beyond prostatic capsule

*T4….carsinoma fixed to adjacent organs

2. Prost. carinoma :{staging: see above}

A). Plain : for bony metastasis (dense deposits).

B.) I.V.U : the same as benign hyperplasia, but the protrusion may have an irregular outline.

C.) Voiding cystogram.:

The prost. urethra may be elongated. Narrow irregular tubular lumen not slit.

D.) Trans.Rectal.U/S:

- Distorted capsule.- Irregular echogenic areas.


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Urology 33

- Prost biopsy.

E.)C.T + MRI: -imp. for extension but not tumour itself ,non homogenous, enlarged

prost with ill defined irregular outline.

- Invasion of fat planes and seminal vesicles.

- Nodal involvement “mainly iliac groups (EXT).

C. Urethral valve obst.

- Occurs only in male.

- Age : mainly infants & childhood.

-C/P : R.F., urinary tract infection, incontenance.

-Types :

.Site : commonly post. urethra at level of verumontanum/vernumonatous? (rounded

projection on post. part of prost. ureth.).

1. Bicuspid valves of mucosal fold.

2. uni-cuspid .. (most common).

3. Incomplete diaphragm : traverse the post. urethra.

.-Radiolog. App: cystogram”:

1. Hypertrophy of muscular wall of the U.B.

2. Trabeculation, sacculation & divert. formation.

3. Post. urethra :- dilated, proximal to site of obst.

- dilatation usually ends abruptly with a convex lower border bulging dawnward.

4. Free valve margin linear filling defect within the dilated urethra.

5. Diaphragm : may be seen traversing post urethra just distal to vernumonatous.

6. Veisco-ureteric reflux may or may not be seen.

7. Hypertrophy of bladder neck spinning top urethra.

General S&S:

*tortous ureters ,dilated system, progresive renal failure*trabeculated UB,diverticulae,residue,reflux,BN hypertrophy

*uretheral dilatation(General+esp. for urethra)

1-dilated….abrupt

2-valve….filling defect or diaphragm traversing


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Urology 34

D. Urethral stricture

Types & causes :

- Congenital false : urethral instrumentation.

true : occurs in boys, at. the junction of bulbous with memberanous urethra

&may be associated with anal atresia.

-Acquired :

1. Traumatic memb. ureth. direct injury .

fracture pelvis .

prost. ureth. instrumentation

following prostatectomy

2. Inflammatory :

- ant - ureth. gonococcal, S.

- post - ureth. gonococaal, T.B., B.

3. Neoplastic: transitional cell papilloma, sq. cell carcinoma.

-Technique of Ex :

-Injection of” umbradil U” in retrograde urethrogram .

-micturating cystogram.

-Radiolog. App:.

a. Narrowed segments of urethra which may be multiple:

- If very short

they may be missed. b. Post inflammatory changes filling of

- Para-ureth glands small cavities, 1-2mm along the side of urethral lumen.

- Cowper’s gland & ducts short narrow channels arising from post. part of the prost.

urethra, diverging from midline as passing backwards.

Vesico ureteric reflux :

-The competence of normal uretero-vesical junction depends on 3 factors :

1. obliquity of intra-mural course of ureter.2. Surrounding bladder musculature.

3. Mucosal flap valve produced by the intra-vesical submucosal ureter.

-Causes :

A. primary reflux :

-generally considered to be cong. anomaly caused by a short intra-mural course of the distal

ureter through the bladder wall.


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Urology 35

B. Secondary Reflux :

1. Cong. anomalies : vesical divert.( if involve orfice).

duplication of ureter (lower moiety.)

ectopic ureter.

2. Cystitis : acute or chronic

3. Bladder carcinoma : infiltration of orifice rigidity reflux.

4. Neurological lesions.

5. Surgical operations on lower ureter.

6. Lower U.T obst.

Diverticulae of the bladder :

-Cong deficiency in bladder musculature.

-V.U. reflux may occur, when they involve ureteric orifice.

Duplication :

-The ureter from lower moiety opens into the bladder above & lateral to orifice of ureter

draining the upper moiety.

This ureter, therfore has a shorter and less oblique course through bladder musculature

less effective valvular mechanism reflux into ureter draining lower moiety.

Cystitis :

-Produces oedema, rigidity & fibrosis interfering with normal valvular mechanism.

- Acute cystitis transient reflux.

- Chronic cystitis permenant reflux.

Bladder Carcinoma :

-Infilteration of neoplasm around ureteric orifice rigidity and incompetence.

Lower U.T. obt.

Reflux is not due to intra-vesical pressure but occur when a para-ureteric saccule involves

ureteric-orifice .

Classification : 4 grades of severity :

-Grade I : reflux confined to lower pelvic portion of a normal sized ureter.

-Grade II : reflux extending up to kidney during voiding with no uretral dilatation.

-Grade III : reflux extending up to kidney in resting state & during voiding with no ureteral dilatation.

-Grade IV : reflux up to kidney with dilatation of upper tract.(International reflux study in children classification….read in Sutton)


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Urology 36

NB :

- Primary reflux has natural tendency to improve at any time during childhood as growth

with bladder wall thickness a greater intra-mural course of ureter & more effective anti

reflux mechanism.

- 80% of grade I reflux improve within 1st few years.

-Technique micturating cystography

Isotope.

Renal Infection:

Non specific :

- Acute pyelo-nephritis.

- Renal and peri-renal abscess.

- Chronic pyelo-nephritis local reflux nephropathy

-Xan thogranulomatous pyelo. nephritis.

Specific :

renal T.B.

Renal B.

Hydatid disease fungal infection.

Acute pyelo-nephritis :-C/P : bacteuria, pyrexia and flank pain& V U reflux.

-Radiolog. app.:

1. Plain : ill-definition of border of kidney.

2. I.V.U: -Usually normal.

- There may be increase kidney size.

attenuation of calyces.

delayed excretion.

dense persistant nephrogramwith little or no pyelogram may be due to tubular blockage by pus “acute suppurative pyelonephritis.”

(no papillary or calyceal abnormality e no cortical loss).

3. U/S, C.T. :

-mainly appear normal.

-Complications :

-Abscess : intra or extra renal.


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Urology 37

Renal and perirenal abscess:

-Cause : mainly complicating acute pyelonephritis.

A.)Renal abscess :

-Imaging:

1. Gives, the radiology. changes of acute pyeloneph.

2. Evidence of a mass displacing collecting. system and deforming the renal outline.

3. Communication with a calyx an irregular cavity similar to T.B.

B.) Perirenal abscess : peri nephric abscess:

- Etiology : 1. Usually results from extension of renal abscess.

2. Or direct extension from duodenal ulcer, pancreatitis.

-Radiolog app:

A) Plain :-Manifestation of involvement of peri-renal spaces :

1. Fixity of kidney ... demonstrated by insp. & exp. films.

2. Loss of definition of psoas outline.

3. Lumbar scoliosis concave to affected side.

4.There may be sympathetic pleural effusion, elevated diaph.copula.

B). U/S & C.T:

1- Mass with necrotic or fluid centre.

2- Thick irregular wall.

3- Obliteration of para-renal space.4- Presence of gas is diagnostic.

C.) Renal angio.

-N.B. *Renal- abscess defect in nephrogram with displacement of the arterial

branches + abnormal vs.

*Perinephric extension enlargement & displacement of capsular Vs.

*Scarring + normal calyces =Vascular aetiology.

*Disruption of normal interpapillary line& reduction of distance bet.upper pole

calyx& adjacent vertebral body.

Chronic atrophic pyelo nephritis : reflux nephropathy :

-Age : child, young adult.

-Causes : infection of kidney associated with reflux.

-C/P : asymptomatic till onset of renal failure or HT.

-Radiolog. App:

A. Plain : - size of renal shadow.

B.I.V.U:1. Renal size normally Lt kidney > Rt……. 1cm.


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Urology 38

if Rt > Lt or Lt > Rt more than 2cm abnormal .

2. Renal outline : irregularity of renal outline due to coarse scarring of renal substance.

3. Narrowing of renal substance thickness inbetween scarring then is localized hypertrophy.

4. Calyceal deformity: pyelonephritic scarring dilatation and distortion of calyces.

5. Evidence of renal failure .

6. V.U. relfux - present in all children.

C. U/S & C.T: all signs of I.V.U.

DD of small sized kidney Unilateral : smooth or irreg. border.

Bilateral : smooth or irreg. border.

Xanthogranulomotous pyelo nephritis :

- Associated stones in 75%.

-Uncommon form of chronic parenchymal inflammation, in which damaged tissue is

replaced by lipid.

-two forms :

A). Focal form uncommon.

forms an inflammatory mass.

I.V.U indistinguishable from a tumour.

C.T

shows, fatty nature of mass.B). Generalised form I.V.U : non functioning kidney.

U/S & C.T. :

1. Large kidney with hydro-nephrosis.

2. Loss of renal outline due to extension into the perinephric space.

3. Collection of pus within dilated calyces.

Remember: - Renal calculus.

- Non fn kid, large.

- Multiple non-enhancing masses (lipid & pus).

Urinary tuberculosis:

-Pathology:

T.B of the lung or bone…...Tub. bacilli via blood stream…… bacilli arrested at the

glomeruli (cortex)…...Bacilli surrounded by tub. Reaction……Tub. foci (usually

bilateral)………Healing in mild infection……Enlargement of foci which coalese together.

Arrested at this stage.

ulceration into the pelvis : ureter, U.B. vas, epidid, sem.vesicles.


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-T.B. affection of kidney may take one or more of following :

1. Miliary TB :

Small, scattered tub. foci. with can not be demonsterated radiologically.

2. Cortical abscess :

Either : healing with small calcified flecks.

rupture into calyceal system ulcero. cavernous type.

3. Ulcerocavernous : ( comonest)

- Rupture of the cortical abscess with extension into calyx.

- Ulceration of the apex of a pyramid.

-Direct extension of disease process destruction of the calyces cavity formation

coalese to attain large size.

4-Tuberculous pyonephrosis :

-T.B infection.

-Spasm, stricture } obstruction at neck of the calyces.

-T.B debris. pelvi-ureteric junction

--- Lower end ureter.

5. Caseo cavernous tupe :

- Extension fo T.B. pyonephrosis involvement of the whole kidney kidney becomes

replaced by number of sacs filled with tub. caseous material.

-Silent extension of process

calcification

loss of the kidney function

“tubeculous auto-nephrectomy.”

6. Tuberculoma : resembling a tumour.

-Imaging:

A. Plain :

Renal outlines :

1. Bulging of renal outline by T.B. cavity or tuberculoma

2. Irregularity of outline with renal size d.t. fibrosis3. Increased in renal size T.B . pyonephrosis

Renal calcification :

Incidence :

- Common in T.B of kidney

- May occur in seminal. vesicle & prost.

- Very rare in T.B of urinary. bladder.

Size :

- Varies from minute deposits to a complete cast of kidneyShape : may be :


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Urology 40

1. Multiple, small punctate calcification

2. Simulating a stone.

3. Calcification in caseo cavernous type :

*Little calcification in caseous material soft fluffy opacities “cummulus cloud”.

opacities “cumulus cloud”

*Extensive calcification dense opacities which gravitate at the buttom of the sac.

Calcification may extend in an irregular manner into the ureter.

B. I.V.U:

a. Ill definition of the minor calyces indistinct feathery outline.

b. Cortical abscess rounded cavity with irregular walls communicating with deformed

calyx.

c. Destruction by fibrosis - Dilatation of the deformed calyces.

- Scarring of renal outline.

d. Cicaterization of calyx :- Stricture and narrowing of calyces with proximal dilatation.

- Complete cut off of the affected calyx.

e. Local tuberculoma -Filling defect and calyceal displacement.

f. Filling defect with dilatation of renal pelvis d.t. caseous debris in the lumen of the ureter.

g. Non functioning kidney due to :

- Destruction of the renal tissue. Or,

- Obstruction of the renal pelvis & ureter by debris.h. ureteral involvement :

1. Irregular areas of dilatation and narrowing with tortous rigid appearance of the ureter.

ii. Ureteral stricture by fibrosis loss of normal curvature the ureter enters the

urinary bladder perpendicular to it with visible widen open mouth “golf hole”.

iii. Uretral stricture hydroureter + hydronephrosis.

I. Bladder involvement “T.B cystitis”:

1. Reduction of the bladder capacity.(Thimble U.B.).

2. Cobble stone appearance : due to oedema of bladder mucosa.3. Filling defect.

4. Gross, irregular contracture of U.B with reflux into dilated ureters in advanced cases.

5. Spotted calcification (rare).

C. Angio-graphic findings :

1. Tub. foci avascular areas.

2. Tub. abscess displacement of blood Vs. arround abscess.

3. Nephrogenic phase scarring of the renal tissues.

D. U/S & C.T :DD causes of unilateral, scarred, small kidney.


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Urology 41

Urinary schistosomiasis :

- Pathogenesis :

- Produced by infestation by schistosoma haematobium.

-The adult worm, inhabits the submucosa of bladder where the ova are deposited…. ova

calcify and excrete a toxin producing tissue necrosis and extensive fibrosis.

-Radiology app.:

1. Plain.

1. Calcification :

- The most diagnostic finding.

- Commonly involves bladder, less commonly lower ureter.

-The appearance of calcification varies according to degree of bladder distension:

*With bladder distended : forms thin linear apacity outlining the bladder margin.

*With bladder empty : forms thick linear opacity or calcified plaque.

2. Stones.

2. I.V.U:

A). Urinary bladder:

- Earliest change ... swelling of its mucosa giving cobble stone pattern.

- In advanced cases .... papillomatous granulomata may form filling defects within its lumen

... carcinoma is a common complication.

B). Ureter : ureteral dilatation and tortuosity even in the absence of obstruction.

*In earliest stages ... dilatation is confined to the lower 1/3 with irregular margin and

granulomata may produce small round filling defect.

* In advanced cases .... the dilatation may involve the whole length of the ureter and the

pelvis.

ureteral strictures ... most frequently in the lower of the ureter hydro-nephrosis +

hydroureter

3. Micturating cystourethrogram :-In early stages normal.

-In advanced stages 1.Decrease U.B capacity with thickened irreg. wall.

ii. Reflux due to fibrosis around the vesico ureteric junction.

iii. Bladder neck obst due to fibrosis.

Hydatid disease:

- Plain : calcification.

- IVP :1. The cysts start in renal cortex have the same radiological picture of simple renal cyst.


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Urology 42

2. The cyst may rupture into a calyx .... so it fill with contrast in I.V.U & daughter cysts

within parent one may form filling defects + sometimes the collecting system communicate

with the space between ecto. and endocyst... so the contrast medium will present in cyst

wall produces an ill defined opacity around cyst.

- U/S & C.T. :

- Shows unilocular or multi-locular cysts with well defined wall and has water density (CT).

- The presence of daughter cysts is diagnostic.

Renal parenchymatous diseases:Classification :

acute and chronic

I. No papillary, calyceal abnormality and no focal cortical loss :

1. glomerulo nephritis.

2. Acute cortical necrosis.

3. Renal vascular disease

5. Acute tubular necrosis.

5. Acute pyelo nephritis.

6. Causes of general infiltration of renal parenchyma e.g. leukaemia.

II. No papillary, colyceal abnormality but with cortical loss :

- Focal infarction. III. Papillary, calyceal abnormality with focal cortical loss :

Chronic atrophic pyelo nephritis (reflux nephropathy) also this occur in TB.

Glomerulonephritis

-Ag Ab reaction (PSGN).

-It means generalised damage to glomeruli.

-The kidney frequently appears normal.

- The only abnormality that may seen ... symmetrical change in size :*acute stage….. swolen kidney.

*chronic stage….. small kidney.

Acute tubular necrosis :

- Acute reversible renal failure acute oliguric renal failure.

Etiology :

-Usually follows episodes of severe ischemia, nephrotoxins

Radiology App.

1. Plain & U/S normal or only swelling kidney.2. I.V.U no filling of the pelvic calyceal system + Persistent nephrogram.


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Urology 43

Acute cortical necrosis:

-Irreversible renal damage.

-Etiology : as acute tubular necrosis.

-Radiological app :

- Acute stage swollen kidney.

- Chronic stage shrinkage kidney.

- Patchy or linear calcification (=tram line calcification).

Focal or lobar infarction :

-Causes : mainly follows occlusion of an interlobar artery, usually caused by an embolus.

-C/P : Renal pain and haematuria.

-Radiolog. app.:

1. Plain & U/S normal.

2. I.V.U:

a. Early changes :

May show focal nephrographic defect with non filling of underlying collecting system.

b. Later changes :

Broad base scar without underlying calcyceal deformity

3. Angio-graphy :

-Arterial block in nephrogram

wedge shaped defect in renal parenchyma.-DD: reflux nephropathy.

TB

Radiation Dysplasia.

Renal papillary (medullary) necrosis:

-It may be acute or chronic.

-Causes ADIPOSE “of acute necrosis”:

A Analgesics (Asprin).D Diabetes (commonest).

I Infants in shock.

P Pyelonephritis.

O Obstruction.

S Sickle cell anaemia.

E Ethanol.

-All the above causes ischaemic necrosis of the pyramides but never extend to cortex.

-C/P : .Haematuria, renal colic, sterile pyuria..Late stage renal failure.


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Urology 44

-Radiolog examination : ( in chronic necrosis):

1-Plain

-Calcification marginal calculus with a radiolucent centre.

calcif. and ossification of a shrinken necrotic papillae.

2. IVU :

a. Kidney :normal or small sized with well defined smooth border.

usually bilateral (85%) with multiple papillae affected.

b. Calyces: will appear dilated following total sloughing of papilla clupped calyces.

c. Papillae may show:

1. enlargement early

2. Partial sloughing fissure forms and may communicate with a central, irregular

cavity loss of loss definition of the calyceal line.

3. Total sloughing :The sloughed papillary tissue may :

a. Fragment and be passed in urine.

b. Remains free in a calyx.

c. Cause ureteric obstruction.

d. Remain in pelvis a ball calculus.

4. Necrosis in situ :

The papillae is shrunken and necrotic but has not separated small kidney.

DD :1. Ch. pyelo-nephritis small, scarred kidney. calyceal deformity but no papillary

sequestration.

2. Renal T.B erosion of papillae ill definition of the calcyceal line.

cavitation is not confined to pyramid.

3. Medullary sponge kidney.

4. Calyceal cyst.

5. Renal stone.


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Urology 45

Haematuria:

Causes :

I. Lesions in urinary tract :

1. Renal :

-Cong. polycystic disease Med. sponge.

-Renal trauma.

-Acute, chronic pyelo nephritis, renal T.B, G.N.

-Renal calculi.

-Renal vein thrombosis.

-Renal masses hyper-nephromas.

pelvis : papilloma, angioma .

2. Ureteric : Stones ,tumour.

3. Vesical : trauma , stone, cystitis, tumours,T B,bilharziasis.

4. Prostatic : prostatitis , S.E.P, malig tumour.

5. Uretheral : Rupture, urethritis , stricture, stone , growths.

II. Disease in the adjacent organs :

-Inflammatory : appedicitis, salpingitis, pelvic abscess spread to wall of U.B.

-Carcinoma : ca rectum, ca. uterus infilteration through bladder wall haematuria.

III. Blood diseases :

-Purpura, haemophilia, leukeamia.

Radiology approach :

I. Plain :1. Abdomen & pelvis:

A.) Kidneys :

i. Site : may be displaced by mass.

ii. Size :*Unilateral, smooth, enlarged kidney :

1. Congenital : fused ectopia, multi cystic kidney.

2. Traumatic : haematoma, urinoma.3. Inflammatory acute deg. glomerulo-nephritis.

acute pyelo-nephritis.

hydro-nephrosis, pyonephrosis.

4. Neoplastic : infilteration as leukaemia, lymphoma.

5. Vascular : renal vein thrombosis.

Acute ischaemia.

*Unilateral, small, sized kidney :

A. Scarred : T.B., ch. pyelonephritis. Infarction.


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Urology 46

B. Smooth : Renal artery stenosis.

cong. hypoplasia.

ch. atrophic obst. Kidney.

renal papillary necrosis bilat.

iii. Contour :

-Localised bulge in renal contour renal mass benign or malignant.

B)Radio-opaque shadow :

1. Renal stone.

2. Renal calcification.

3. In course of ureter stone .

calcification upper 1/3.

lower 1/3 “trame line” Bilharziasis.

4. In site of U.B stone.

calcification in wall B.

calcification in seminal vesicle T.B.

calcification in prostate tumour , concretion.

C)Retroperitoneal facial planes (psoas line):-

-is obliterated when involved by inflammatory or infilterating process.

D)Spine and bone pelvis :

- Osteolytic lesions.

- Osteoplastic lesions prostate.

- Scoliosis in renal infections.

- T.B of spine.

2. Plain X-ray chest :- Lung TB : as renal T.B is usually 2ry to lung.

- Metastasis : canon ball of hypernephroma.

- Rt side heart failure renal congestion haematuria.

- Poly cystic disease “involving lung.”

- Lymphoma with renal involvement.

II. I.V.U :

1. Excretion of the contrast :-Poor renal vein thrombosis & renal artery stenosis.


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Urology 48

Value :

1. It can define the site, size and contour of kidney.

2. Detection of calyceal dilatation.

3. Cortical thickness.

4. Calcification and stones highly echog. + acoustic shadow.

5. Any mass lesion size, site, outline well defined.

ill defined.

echogenicity : cystic of solid or mixed.

6. Detection of metastasis + lymph nodes in malig. Lesions.

7. Guided biopsy.

IV. C.T. :

- Used in equivocal ultrasonic finding.

- Can asses site, size, outline, attenuation, value, calcification and enhancement pattern of

any mass.

- Detection of extra renal extension of lesion

- Vascular elements renal vein, I.V.C.

- Lymph nodes + retro-peritoneal structures.

V. Angiography :1. For vascular lesions haemangioma of kidney.

renal artery aneurysm.

2. Vascular involvement in malg. tumour.

3. For embolectomy in life-threatening haematuria.

4. Before partial nephrectomy(= preoperative).

VI. Isotopes scanning.

VII. MRI.


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Injuries to genito-urinary tract:

1. Urethra : Anterior uretheral injuris( penile= extrapelvic):

-Etiology :Direct trauma e.g. crushed against floor of pelvis staddle injury.

-C/P :

Haematuria, inability to void.

-Types of injury :

1. Contusions : there is no mucosal tear.

2. Partial & full thickness mucosal tear, but there is some mucosal bridging.

3. Complete.

-Radiolog. app.: “Ascending urethrogram”: a. If buck’s fascia is intact extravasation in penis & scrotum.

b. If buck’s fascia is disturbed extravasation in abdominal wall.

2.Post urethra : prost. & memb. = intrapelvic:

-It is more common & usually associated with pelvic fracture.

Etiology :

-Direct force.

-Shearing force : acceleration & decelation due to difference in mobility of membraneous

and prost. Urethra.

Types of Injury: (Based on urethrographic findings):

-Type I : Post. urethra is stretched 2ry to hoematoma in the prost. bed.

-Type II : prostate & urethra are disrupted.

extra-vasation is supra-diaphragmatic (urogenital diaphragm).

-Type III : Injuries both in membran, urethra and urogenital diaphragm.

Extra-vasation & hoematoma extend to proximal bulbous urethera.

Radiolo. appearance :

1. Fracture pelvis.

2. Urethrogram:

-Type I : stretching of the prost urethra with no extra-vasation

-Type II : extra-vasation of C.M. into pelvic extra-peritoneal and limited inferiorly by

intact urogenital diaphragm.

-Type III : extra vasation above and below the diaphragm.


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2. Kidney :

-Etiology:

- Penetrating trama .g. knife, gun, shot.

- Blunt trauma.

- Iatrogenic trauma

at surgery. percut. nephrostomy.

-Predisposing factors :

- Mobile kidney.

- Hydro-nephrosis, tumour, cyst.

-C/P :

- History of trauma.

- Haematuria.

- Flank : tenderness, contusion, palpable mass.- Shock.

-Classification of renal injuries :

1. Mild “minor”.

2. Mjaor ‘severe”.

3. Catastrophic.

1. Minor :

-C/P : - Haematuria, normal vital signs.

- Palpable flank mass.

-Pathology :

-Contuion of kidney with minor cortical laceration without disruption of the pelvi

calyceal system.

-Radiolog. app.:

A. plain : normal.

B. I.V.U. : usually nromal.

C. U/S : renal contusion appear as cystic or non cystic according to age.

D. C.T. : fresh contusion relatively hyper-dense.

older one hypodense.

E. Angio: normal.

2. Major :

- Haematuria + unstable vital signs.

- Palpable flank mass.

- Perinephric or para-nephric haemotoma.

Pathology : -Cortical laceration through capsule or into pelvi caly. Syst..


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Radiolog app.:

A. Plain :

1. Lower rib fracture.

2. Fracture of tr. proceses of lumb verteb.

3. Loss of definition of peri-nephric tissue.4. Focal loss of psoas line.

5. Elevation of hemidiaphragm on same side.

6. Scoliosis with convexity to opposite side due to contraction of psoas muscle.

B. Urography :

1. Enlargment of the renal outline.

2. Nephrotomography with high dense C.M. is imp.:

- Complete cortical laceration.

- Extra-vasation of C.M. into renal parenchyma. peri-nephric.

subcapsualar space.

3. Calyceal laceration may occur extravasion of the C.M.as above.

( N.B. Chronic urinary extravasion Urinoma)

C. U/S :

- Perinephric or para-nephric hypoechoic or hyper echoic collection.

- Change in size of the kidney.

-Tear in the kidney, pelvi-caly, system as hypoechoic line within the renal

parenchyma.

D. C.T :

- Deep parenchymal laceration.

- Peri-renal Hge hyperdense.

- Extra-vasion of C.M either into pararenalspaces renal parenchyma.

- Associated liver or splenic injures .

E. Angio-graphy :

-

A sub-capsular hoematoma, will cause stretching of the capsular

vesseles around haematema.

3. Catastrophic :

-C/P : unstable vital signs, shock + haematuria.

-Pathology : - shuttered kidney.

- pedicle injury renal artery avulsion .

renal thrombosis.

-Radiolog. app.:

a.Plain: as major.

b.Urographic: partial or total renal impairment


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c.U/S: as major .

d.C.T: - shuttered kidney.

- multiple fracture planes separating functioning renal fragment.

e.Angio-graphy:

- pedicle injury

renal occlusion. avulsion (DD : renal spasrn if less than 2hr. after trauma).

thrombosis.

-Complication of renal injury :

A. Immediate : occur within 6 weeks

1. Hge

2. Sepsis due to peri-nephric abscess or acute pyelo nephritis.

3. Fistula formation.

4. Significant urinary extra-vasation “grades”:-Grade I : intra parenchyma.

-Grade II : beyond renal capsule but confined to the Gerota’s fascia.

-Grade III : free retro-peritoneal extra-vasation.

B. Delayed :

1. Hypertension due to ischaemic fragments of renal parenchyma.

2. AV. Fistula.

3. Post traumatic pseudo-anaurysm.

Complications of renal transplantation:

-The transplanted kidney is usually placed in the iliac fossa & the renal vessels are

anastomosed to the Ext. or internal iliac A.

1. Rejection : hyperacute, acute, chronic:.

-Clinically : malaise, tenderness, oliguria, serum creatinine.

-Radiology app. : (-Isotope + US first choice. )

(-Angio transplant renal a. stenosis).

a. 99 Tcm DTPA :

- Poor perfusion serial scan + flow index.

- Delayed scans progressive tracer accumulate in transplanted with little

bladder activity.

- Pseudo obstruction : upper tract is dilated, tracer reach U.B. and respond to

frusemid DD obstruction.


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b. U/S :

1- Renal swelling.

2- Large hypo-echoic pyramids, which indicate infarction and necrosis.

3- Hyperechoic cortex.

4- Indistinct cortico-medullary junction.c. Angiography :

1. Poor filling of cortical vesseles leofless tree appearance.

2. Delayed arterial washout C.M.

3. Stretched intra-renal Vs.

2. Acute tubular necrosis:

- A major cause of renal failure Immediately post operative.

Normal pelvic index. Background.

Prol

Master Radiology Notes Urology

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