Urology 1

URORADIOLOGY

Congenital 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.

Congenital HYDRONEPHROSIS (see pediatric abd.)

Q:CONGENITAL ANOMALIES?:
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 in
undifferentiated 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 peri- portal 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:
Multicystic: dysplasia undiff. Tissue inbet….atretic.
Adult polycystic: AD 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 pelvi- calyceal 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 gradualuptake in
the collection.
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Renal Neoplasms:
A) parenchymal renal 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 1confined 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.
-Blood cannon ball metastases(more common)
-Lymphatic

Malignant renal cell carcinoma

Adenocarcinoma (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 phase
of 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 peri- renal 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 involvement :

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 &necrosis
MICROSCOPE:
* 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 diseaseureteric 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 pelvisfilling 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.
 Urology 18

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
 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 filling 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 stricture :
1-T.B. 2-Bilharziasis.
3-Sq. cell carcinoma. 4- Ureteric involvement by retroperitoneal disease.
 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.UT
I. 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.
 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
 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 20-30y
2. Site : trigone lateral side then spread
3. Macrocop.  papillary -Nodular fungating mass
 nodular -malig ulcer
 ulcerative -diffuse infilteration
4. Microscopic : transitional cell 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.
 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
-Effect :
- Urine stasis  infection & stone formation.
- Reflux  if ureteric orifice lie inside diverticula.
- Obstruction of lower ureter by a large diverticula.
-Micturating 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.
 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 :
 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 matrix
covered 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 :
 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. Medullary 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. Cortical 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.
 Urology 27

C. Dystrophic calcification due to localised 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.
 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 -Renal size  or 
-Modest renal enlargement -Faint nephrogram no pesistant
-delayed calyceal nephrogram
opacification(pyelogram) -Parenchymal thickness
-dilated pelvis & ureter (up to obst) -Massive hydronephrosis(+dilated tortous
-pyelosinus extravasation ureters&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.
 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, parallel
to 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.
 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 diverticulae
6. Vesical residue.
 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.
Incidence & 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. *433.8cm (2=calculated weight).
*average wt 20gm.
*benign hypertrophyperiurethral central zone.
 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.
 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: cysto-gram”:
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
 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.
 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)
 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.
 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.
 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.
 Urology 39

-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. fibrosis
3. 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 kidney
Shape : may be :
 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.
 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.
 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.
 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.
 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.
 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.
 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.
 Urology 47

-Non function kidney  traumatic.

 cong. multi cystic kidney.
 neoplastic  destruction by tumour.
 occlusion of renal vien.
 inflammatory  T.B acute nephropathy.
 cortical necrosis.
2. Calyceal system :
- Distortion : T.B, ch. pylonephritis.
- Amputation : malignant process.
- Enlargement : obst. by stone, stricture.
- Cavity formation ; in T.B calyceal cyst.
- Displaced, stretched by a cyst.
- Inter-papillary line :
* Irregular  scarred kidney malig. Process.
* Smooth  normal, enlarged or small kidney.
- Thickeness of renal cortex :
*Smooth, thin  obst. atrophic.
*Irregular  scarred kidney.
3. Renal pelvis :
- Dilated  obst. by stone, stricture.
- Filling defect ... as before “see pelvic tumour.”
4. Ureters :
-Course , calibre, strictures and reflux.
5. U.Bladder :
-Capacity:  in contracting bladder  T.B, Bilharziasis.
 ch. Inflammation.
 tumour.
- Filling defect  as before.
- Post. voiding  residual urine in prost. enlargem.
6. Micturating urethrogram :
- Uretheral injury  leak of contrast into perineum.
- Urethral strictures.

III. U/S:
- Abdominal  renal + bladder lesions.
- Trans-uretheral  bladder + prostate.
- Trans-rectal  bladder + prostate.
 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.
 Urology 49
____________________________________________________________________________________________________
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.
 Urology 50
____________________________________________________________________________________________________
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..
 Urology 51
____________________________________________________________________________________________________
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
 Urology 52
____________________________________________________________________________________________________
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.
 Prolonged T.T.
 Urine out put is scanty & late.
-Radiolog. App:
a. Tc99m D.T.P.A : A good perfurson with poor uptake (D.D. rejection).
b. U/S:  normal.
c..I.V.U : Increasingly dense persist nephragram dt. leakage of tubular filterate
through damaged tubular wall.
 Swollen kidney.
 Elongated calyx due to renal oedema.

3. Fluid collection :
A. Lymphocele .
- Typically, it is inframedial to transplanted kidney.
- Reuslt from leakage of lymph from interrupted lymph vesseles of doner or recep.
Kidney.
-Radiolog. app.:
- 99Tcm D.T.P.A:  cold area.
- U/S:  fluid collection (hypo-echoic) with septation

B. Urinoma.
- Extra-vasation of urine from site of implantation (from U.B or ureter) or from donar
kidney into retro-peritoneal.
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-Radiolog. App:.
a. 99Tcm D.T.P.A:  extra-urinary hot spot .
b. U/S :  Fluid collection, may be septated.
c. I.V.U, cystography, retrograde urography :  to detect the site of leak.

4. Obstruction :
-Causes :
a. - Ureteric stenosis :  aedema at site of implantation of U/B.
 fibrosis
b. Fluid collection:  pressure.

5. Occlusion of the renal vesseles.

Renal Ischemia:

-Etiology :
1. Aortic diseases : atheroma, dissecting A. , Aneurysm, thrombosis.
2. Renal arterial diseases.
a. Atheroma :
- The commonest lesions.
Commonest: - Usually involves the orifice or the proximal 1/3 of the main
artery.
- May be bilateral 30%.
b. Fibro-musculo, hyperplasia (string of beads)
- Bilatr in 50%.
- Young women.
- Usually affects the middle and distal 1/3 of the artery.

c. Thrombosis or embolism.
Less common : d. Compression by tumour.
e. Aneurysm, angioma.

Radiology app. of renal a. stenosis:

A. I.V.U:
1. Decrease in the renal size:
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- Is the most reliable index of renal ischaemia.
- It may be due to  reduction in the renal fluid volume as a result of  blood flow
or ischaemic atrophy of renal tissue.
- Stenosis affects the main renal artery  uniform reductison in size.
- Occlusion of a segmental artery  reduction inrenal thickness of that segament.
- Occlusion of small renal arterial branches  multiple infarction  scarring of the
renal outline (DD. Ch. pyelo-nephritis).
2. Delayed in excretion :
-A small, non-functioning kidency with a normal retro-grade urogram 
charactaristic of acute complete obst. of artery.
3. Increased concentration of contrast media:
- Renal ischaemia   tubular reabsorption of Nacl & water   cencentration of
tubular fluid with  its volume  progressively increased density of the calyces.
4. Reduction in  size of collecting system :
-small, dense collecting system is due to  quantity of urine + atr.
5. Ureteral notching :
- Ureteral indentation by the development of a collateral circulation through the
ureteral arteries from the lumbar branches.
-Usually seen in upper ureter.
-Digital subtraction angio.

B. Renal angiography (Digital subtraction angio):

- Indication : 1. Pre operative + balloon dilation.
2. In hypertensive patient < 30s.
3. Rapidly accelerating hypertension in patient > 40 yrs.
- Aortogram at just to see origin of renal as + aberrant renal A .
- Then selective  atheroma  proximal narrowing.
 dysplasia  string of beads.
C. Isotope.

Renal vein thrombosis :

Etiology :
-Usually 2ry to invasion of the vein by renal tumour or retro-peritoneal tumours.
-It may occurs, when renal blood flow is ↓ as in glomerulonephritis & pyelo-nephritis……
1. Nephrotic syndrome GN, DM, SLE , Amyloid.
2. Cyanotic HD.
3. Hypovol shoch.
4. Hyperviscosity synd..
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5. Extension of tumour.
-C/P :
Acute complete occlusion presents e:
 sever loin pain, fever, haematuria, leucocytosis.
 pulmonary emtoli are common 33%.
-Rad. Appearance:
A. I.V.U( Like renal a. stenosis but small kidney):
- Acute complete occlusion  large, non functioning kid.
- In gradual occlusion : a collateral circulation develops  non
impairment of the renal function  alrage kidney with a poor persistent
nephrogram, elongation & splaying of the calyces, ureteral notching by collateral
circulation.
B. C.T:
- Direct demonstration of thrombus within a dilated vein.
- Renal enlargement & peri-renal venous collateral.
C. Renal angio graphy:
-In acut stge:
 Poor persistent nephrogram.
 Flow through renal art. branches.
Non opacification of renal vein.
D. Renal phelbography :
- Thrombosis of I.V.C must be Excluded before doing selective renal vein catheterization.
E. US:
- Hypoechoic  acute.
- Echogenic  10 days.
- Loss of cortico medullary differentiation.
- Absence of doppler venous signal.

Retro peritoneal fibrosis:

- A disease of unknown etiology in which there is a proliferation of fibrous tissue in the

retro-perit space.
- The process may involve any structrure in the retro-per, space e.g. I.V.C, iliac veins,
aorta, renal artery, C.B.D.
- The fibrosis may extend downwards into the pelvis and upward through the diaphragm
crura to involve the mediastinum.
- Radiolog. app.:
A. I.V.U :  medial ureteral deviation and obstruction .
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- A characteristic feature is that a retrograde catheter can be passed easily
through the obst. segment.
B.C.T :
- Diffuse sheath of soft tissue density  enasement of aorto ureter.
 infilterating retro-peri. Fat.
- or single or multiple masses may seen resembling retro-pert tumour.
- C.T guided biopsy  provide the histology. features.
C. Phlebography :
-May demonstrate obst. of I.V.C or iliac veins.

-DD:of causes of ureteral distortion and obstruction:

1. Retro-perit malignancy : lymphoma, metastasis from colon, breast.
2. Inflammatory condition : crohn’s disease, divert. disease, pancreatitis.
3. Aortic aneurusm.
4. Trauma fibrosis occurs secondary to blood in the retroperit. tissue.
5. Surgery
6. Drugs
7. Idiopathic : 75%

N.B.: Renal failure :

(1) Is it acute or chronic  size of kidney.
(2) Is there evidence of obst.
-U/S  answer both
- Acute or chron.  Renal size
- Obstr,  ? pelvicalyceal dilation
- IVP , C.T., Isotope  Supplementary

Differential diagnosis:

Gas in the urinary tract :

 Gas inside bladder :
1. Vesico-intestinal fistula : divert. disease, carcinoma, of colon or rectum.
2. Cystitis : due to gas forming organisms e.g.E.coli esp in D.M.
3. Following instrumentation.
4. Penetrating wound.

 Gas in bladder wall :

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- Emphysematous cystitis : usually in D.M.

 Gas in ureters and pelvicalyceal systems

1. The above causes trauma instrumentation.
2. Ureteric diversion into colon or bladder.
3. Fistula : perforated duod ulcer, crohn’s disease.
4. Infection : esp. in D.M.

Non visulaization fo one kideny during I.U.U:

1. Absent kidney : congenital or post-nephrectomy.
2. Ectopic kidney.
3. Ch. obst. uropathy.
4. Infection : pyonephrosis, T.B.
5. Tumour : tumour completely replacing the kidney or occluding the renal vein or pelvis.
6. Renal artery occlusion  ..................... important.
7. Renal vein occlusion acute  ............... important.
8. Multi-cystic kidney.

Causes of small, smooth kidney:

A. Unilateral : with compensatory hypertrophy of other kidney.
1. With a dilated collecting system .
-post-obstructive atropy + thinning of renal cortex (famous).
2. With a small volume collecting system.
This is asign of diminished urinary volume +
i. Delayed opacification of calyces.
ii.  Density of opacified collecting system. Indicate ischaemia.
ii. Delayed wash-out following diueretics.
a. Renal artery stenosis.
b. Radiation nephritis : at least 2300 Rad 5 weeks. +/- other sequelae of radiotherapy
e.g. scoliosis in children.
c. End result of renal infarction.

3. With 5 or less clayces.: – Cong. Hypoplasia.

N.B.- Unilat / small / scarred :

1. Reflux nephropaity : GN.
2. TB.
3. Lobar infarction.
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4. Renal dysplasia.

B. Bilateral .
1. Generalised arterio sclerosis  Normal calyces.
2. Chronic glonerulo - nephritis.
3. Chronic papillary necrosis.
4. Arterial hypotension.
5. Causes of unilat. small kidney occuring bilaterally.
N.B. Small kid. large kid. ( Uni or / bilat.)
 
persrs obst. Cong.
RAS Trauma
Radiation Inflamation
Renal infarction Vasc
Cong. hypo plasia Miscell
Ch. GN and papillary necrosis,
ch focal pyelonephites (reflux)
TB
Infarction
Dysplasia

Causes of large smooth kidney:

A. Unilateral :
- Congenital : duplex kid, fused crossed ectopia, multicystic kid, adult poly cystickid.
- Traumatic : haematoma, urinoma
- Inflammatory : -Pyonephrosis, actue pyelonphritis
-Obstructed kidney  (hydronephrosis)
- Neoplastic infiltrations eg. leuk.
- Vascular : renal v. thrombosis.
- Compansatory hypertraopy.
B. Bilateral :
I. Proliferative & necrotizing disorders:
1. Acute glomerulonephritis.
2. Polyarteritis nodosa, S.L.E
3. Good pasture’s diseasse actue Haematuria GN + pulm. Hge.
II. Deposition of abnormal proteins:
1. Amyloid.
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2. Multiple myeloma.

III. Abnormal fluid accumulation :

1. Acute tubular necrosis.
2. Acute cortrical necrosis.
IV. Neoplastic infiltration:
Leukaemia & lymphoma.
V. Inflammatory cell infiltration:
Acute interstitial nephritis.

N.B.Cong : inf polycystic medullary sponge kid

Tramua :
Inflamma : hydronephrosis , acute GN, TN & PN
Neopl : leukc, lymphoma, MM
vasc : renal V thrombosis
Miscell : Amyloid, acromegally.
VI. Miscellaneous :
1. Renal vein thrombosis.
2. Acute renal papillary necrosis.
3. Infantile polycystic disease.
4. Sickle cell anaemia.
5. Bilateral hydronephrosis.
6. Medullary sponge kidney.
7. Acro-megally.

Causes of localized Bulge of renal outline:

1. Simple cyst.
2. Tumour+ Pseudo tumour.
3. Fetal lobulation.
4. Dromedary humb.
5. Splenic impression.
6. Localised hypertrophy.
7. Abscess.
8. Enlarged septum of Bertin.
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Causes of unilateral scarred kidney (small):

1. Reflux nephropathy : a focal scar over a dilated calyx. ( V.Imp.)
= Chr. pyelonephritis : - usually multifocal.
- Scarring is most prominent at upper & lower poles.
2. T.B  calcification.
3. Lobar infarction  normal inter-papillary line (scanning over normal calyx).
4. Renal dysplasia  normal sized kid.

DD :
-Persistent fetal lobulation (  normal size kidney)
-Normally : cortex parallel to interpapilary line.
-Lobar infarction: broad depression over normal calyx.
-Reflux nephropathy: focal scar over dilated calyx.

Nephrographic patterns:

A. Immdiate faint persistent nephrogram:

1. Proliferative necrotizing disorder  as before acute GN.  AGN
2. Renol vein thrombosis.
3. Chronic severe ischaemia.
B. Immediate distinct persist nephrogram:
1. Acute tubular necrosis.  ATN
2. Causes of acute renal failure.
3. Acute hypotension.
C. Increasingly dense nephrogram:
1. Acute obst.  Obst., RVT
2. Acute hypotension.
3. Acute tubular necrosis.
4. Acute pyelonephritis.
5. Renal vein thrombosis.
6. Multiple myloma.
7. Acute papillary necrosis.
D. Rim nephrogram:
1. Severe hydro-nephrosis.  Hydro
2. Acute complete arterial occlusion.
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E. Striated nephrogram:
1. Acute ureteric ob.
2. Infantile polycystic disease.  Inf PCK
3. Medullary sponge kidney.
4. Acute pyelonephritis.

Filling defect in renal pelvis or acalyx

a. Technical : overlying gas shadow.

b. Extrinisc with a smooth margin:
1. Cyst.
2. Vascular impression as intra-renal A.
3. Renal sinus lipomatosis
4. Collateral vessels in renal A. stenosis.
c. Inseparable from wall and with smooth margins:
1. Blood clot  may be adherent to wall or free in lumen.
 change in size over several days.
2. Papilloma.
3. Pyelo-ureteritis cystica  due to ch. Infection.
 multiple, well defined submucosal cysts.
d. Arising from wall with an irregular margin:
1. Transitional cell carcinoma.
2. Sq. cell carcinoma.
3. Renal cell carcinoma.
4. Cholesteatoma.
E. In lumen:
1. Blood clot.
2. Lucent calculus.
3. Sloughed papilla.
4. Air.

Dilated ureter:
(Don’t Forget Stone, Reflux)
A. Obstruction :
1. Within lumen:
a. Calculus.
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b. Blood clot.
c. Sloughed papilla.
2. In wall:
a. Oedema or stricture due to colculus.
b. Tumour.
c. T.B stricture & inflammtory.
d. B.
e. Ureterocoele.
f. Mega-ureter = functional dilat. Of distal ureter.
3. Out side wall:
a. Retro-perit fibrosis, endometriosis, pregnancy.
b. Cancer cx or bladder, prostate.
c. Retro-caval ureter,  on right side only.
 the distal ureter lies medial aL3 to dilated
proximal portion.
 abnormal dev. of IVC (not ureter).
B. Vesico - ureteric reflux.
C. No obst or refulx. : 1. post portum.
2. Following relief of obst.
3. U.T. infection.

Filling defect in bladder : ( same as ureteric obst + prostate)

1. Neoplosm.
2. Prostate.
3. Blood clot.
4. Calculus.
5. Ureterocele (imp)
6. B.
7. Urethral or supra pubic catheter.
8. Endo-metriosis.

Bladder calcification :
A.) In lumen  calculus.  F.B.
B.) In wall  -Transitional call carcnima.  0.5%
 linear, stippled, punctate
 no extra vesical calcif.
- B.  Thin, curvilinear calcification outline the bladder (normal size &
shape)
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 calcification spread to involve distal ureter.
- TB  the disease begin in kidney then spread distally ( versus. B).
 contracted bladder =Thimble UB.

Bladder fistula :
a. Congenital:
 Etopia vesica.
 Imperforated anus (high type).

b. Inflammatory:
 Diverticular disease, crohn’s disease.
 Appendicular abscess.
c. Neoplastic :
 Carcinoma of colon, bladder, ovary.
 Radiotherapy.
d. Trauma .

Infertility:
Definition : difficulty to conceive.
(N.B Sterility : impossibility of having children).

Etiology :
A. Male factors :
I. General II. Local factor
1. Old age. 1. Cong. penis : small - Hypospedius.
2. Obesity. 2. Traumatic .
3. Endocrine problem: 3. Inflammatory: gonorrhoea, TB.
-hyper parathryroidism. 4. Neoplastic of testicles.
-pituitary disorder.
4. Psychological factor.
5. Addiction, alcoholism.

B. Female factors :
I. General II. Local factor
1. Constitutional diseases : TB, 1. Introital factors.
leukaemia. 2. Vaginal factors:
2. Nutritional deficiencies. abscess, stenosis.
3. Obesity. 3. Cx. Factors:
4. Psychological factor. cong., traumatic, inflam, tumour
5.Intoxication–alcholism-lead 4. Uterine factors: as cx.
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poisoning. 5. Tubal factor : cong., inflam.,
6. Endocrine factor: tumour.
-myxoedema. 6. Ovarian factor :as 5.
-hyperprolactin.

Radiolog. methods of investigation :

A. Plain radiography :
1. Of abdomen:
i. Soft tissue mass of pelvis or abdomen.
ii. Ascitis  Meig’s $.
iii. Evidence of neoplastic involvem of spine & pelvis.
iv. calcification:
- Ut fibroid  patchy calcification.
- Ovarian dermoid  teeth.
- N B ovarian fibroma  pl. effusion + ascitis = Meig’s $.
- T.B. pyosalpinx  Amorphous calcification.
- Vas deference, seminal vesicle calcification in male.
2. Of chest:
- Chest TB  infertility due to  Toxic effect.
 T.B. salpingitis.
- Metastatasis :
-Trophoblast. tumours e.g. chorio carcinoma.
 discrete masses.
 or milliary appearance.
 arterial embolization.
- Plural effusion: in Meig’s syndrome.
3. Of skull: for pituitary fossa for detection of pituitary tumours.
B. I.V.U:
1. Pelvic mass compression:
 fundal impression on bladder.
 deviate ureters.
 ureteric obstruction.
2. Invasion of the U. B. by adjacent neoplasm : uterus, cx., ovarian.

C. Cystogram : to investigate stress incontinence or vesico-ureteric reflux.

D. Ba. Enema : to demostrate bowel involvement.
E. Hystro-salpingography : Indications, contra indications, normal H.S.G. (in 1st part).
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Abnormal H.S.G. (Q): 1-Uterus:

1. Congenital anaomalies of uterus :
Various degree of failure of fusion of mullerian ducts  series of congenital
abnormalaties:
a.Ut. didelphus (double ut. ,cx.&vagina).
b.Ut. bicornis bicollis (close connection at cx.).
c.Ut. bicornis unicollis (2 body +1cx.).
d.Ut. unicornis unicollis(+/- rudimentary horn).
e. Septate Ut.
f. Arcuate Ut.
2. Acquired disease of uterus :
b. Endometriosis : the presence of endomet. tissue outside the endomet. lining
of uterus e.g. myometrium.
U/S :- Irregular cystic spaces (cyst within cyst appearance)
- Chocolate cyst.
c. Physiological fluid  rupture follicle.
d. Ectopic pregnancy.
e. Ovarian neoplasm.
f. Fluid filled bowel loop.
g. Appendicular abscess.

II. Ovary :
2. Demonstration of normal ovary with its characteristic pattern of follicles (3 x 2 x
2cm).
3. Demonstration of ovarian pathology : (tumours)
Tumours of ovarys:
a. Epithelial origin :
 Benign :
- cyst : serous cyst adenoma.
 mucinous cyst adenoma.
 simple cyst.
- solid : papilloma.
 Malignant:
- primary : -solid .
-cystic: Papillary serous cystadeno carcinoma.
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 Pseduo mucinous adeno car.
 Epidermoid carcinoma.( Dysgerminomas).
- secondary : Krukenburg tumour from G.I.T or stomach.

b. connective tissue :
- Benign : fibroma + pl. eff and ascites = Meigs $.
- Malig : sarcoma.
c. Teratoid : - dermoid : benign cystic teratoma.
- chorio epithelioma.
N.B. cystic ovarian tumours + non neoplastic cyst :
 luteal
 follicular (MEF)
 chocolate endometrial cyst
(+ stein leventhal synd.)

-Uterine adhesion  Asherman syndrome.

a. Uterine fibroid  see later
b. Pregnancy or missed abortion  irregular filling defect.
c. Exta - ut , pregnancy : sac of foetus is away from uterus.
d. Uterine tumour  irregular filling defects.
e. Para-metrial masses  displacement of tube
f. Vesicular mole  grapelike fillings defects.
g. Fallopian tubes abnormalities:
1. Salpingitis :
 Hydrosalpinx : filled distorted tube.
 T.B salpingitis obst. distal end &when the tube fill  irregular caliber &
small filling defects and may be calcification.
2. Tubal blockage. causes :
i. Fault technique.
ii. Tubal spasm  amylnitrate.
iii. Obst. following tubal infection  fibrosis.
iv. Fimbrial adhesion  filling of tube but no perit. smear.
v. Tubal pregnancy.
vi. Sterilization procedures.

F. Ultra-sonograpy :
1. PID.
2. Ovary:  moraml , mass, function.
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3. Uterus:  congenital, adenomyosis, tumours , hydrocolpus.

I. Diagnosis of pelvic inflammatory disease: e.g. gonacoccal or T.B salpingitis or oophoritis.

The ealist sign of acute uterine infection  thickening of uterus, adenexa with traces of
fluid in peritoneal recesses. progressively tubo-ovarian or pelvic abscess will be formed.

Ultrasonic features of ovarian tumours (also cystic mass).

Benign Malignant
1. Size < 10m > 10cm
2. Wall smooth irregular, poorly defined
3. Locules uni or multilocular with septa - complex with solid compon
4. Debris -ve - + ve echogenic
5. Effect mass effect Ascitis, metastasis
empty abd. appearance Nodules or nodes
6. Movement mobile Fixed to pelvic wall or
omentum.

4. Monitoring of ovarian function :

During each menstrual cycle, one follicle becomes dominant and enlarges. At ovulation its
size arround 2cm (MGF). Serial U/S charting follicular growth  accurate prediction of
ovulation .

III. Uterus :
5. Demonstration of uterine pathology :
a. Cong anomlies as before + Hystero U/S
b. Adeno myosis :
Small poorly echogenic(= hypoechoic) foci in uterine wall  thickened uterine wall
due to hyperplastic endomet. tissue, peneterating the myometrium.
c. Tumour of uterus : (It is best diagnosed by trans-rectal U/S).
1. body:  benign  epith. : adenoma
 non epith. : fibroid leiomyoma
 Malignant  Epith. : Adenocarcinoma
 non epith : leiomyo sarcoma.
2. Cx :  benign : rare.
 malignant :  sq. cell. carcinoma 95%
 adeno-carcinoma 5%
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d. Hydro & metrocolpus : accumulation of fluid or blood in uterine cavity and vagina due to
labial fusion or imperforate hymen. Commonly occurs in young female.

G. C.T.:
Is used in: -suspecious ovarian, cervical or body malignancies for staging and
lymph node invasion, ascites, calcification.

H. Lymphography :
For visulalisation of lymph nodes in uterine carcinoma.

I. Angiography .
J. M.R.I.
MRI : hypo  junctional zone
Fibroid  low on both if bright  redeg. endom, cancer
Cancer  bright on both
Endometrisois  bright on both
Ovray  bright follicles on T2.

Uterine fibromyoma
-It is a benign lesion of the uterus and are mostly oestrogen dependant.
-Pathology :
- N.E.A polyp : 1. Sub serous type.
2. Submucous type.
3. Interstitial type.
- M.E  liomyoma (fibrous tissue + muscle).
-C/P : Bleeding, discharge, infertility and pain.
-Radiolog. Examination :
1. Plain “abdomin” : soft tissue swelling in the pelvis, patchy calcification.
2. H.S.G according to type :
i. Sub-mucous type  multiple, polypoid or single smooth filling defect.
ii. Interestitial type  bulky uteriaus, distortion
iii. Sub. serous type  may be normal or effect of pressure may be seen.
3. Cysto gram :
- Fundal impression on bladder.
- Large fibroid  deviation or obst. of ureters.
4. U/S :
- Masses in or arising from myometrium.
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- Usually homogenous & hypo echoic, show a whorled stromal appearance.
- Hge & necrosis  anechoic areas or hetregenous appearance.
5. C.T +MRI: -Only done in suspected cases.
DD : Of pelvic masses (supra pubic masses):

1. Bladder  acute & chronic retention.

 cancer bladder.
2. Pelvic abscess.
3. Uterus : pregnant, malignant.
4. Ovarian : benign & malignant lesions.
5. Retro peritoneal masses: - Ectopic kidney.
- Huge spleen.
- Chordoma.
- Rhabdomyosarcoma.
The most common causes :
- In female  gravid uterus, U. Bladder retention.
- In male  urinary bladder retention.
-Scheme for pelvic masses :
1. History :
-Pregnancy  amenorrhoea.
-Fibroid  amenorrhoea.
-Urinary blad  retention of urine
 frequency, urgency, dysuria  blad carcinoma
-Ovarian  menstrual disturbanes.
 infertility
2. Plain :
-Soft t. swelling in all.
-Calcification :  fibroid : patchy.
 teratoma : teeth.
-Foetal parts in pregnancy.
-Pelvic and lumbar spine metastases in tumour.
3. H.S.G :
-Filling defect:  smooth  preg. or fibroid.
 irregular  preg or cancer uterus.
-Displacment.
4. I.V.U:
-Ectopic kid.
-Distended bladder.
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-Filling defect in bladder  bladder carcinoma.
-Smooth indentation on fundus of bladder  fibroid.

5. U/S :
-Pelvic abscess : fluid collection in the pelvis.
-Fibroid : ,,, as before.
-U. bladder :  retention : distended, smooth, U.B
 carcinoma : mass as before.
-Retro-peitoneal mass.
N.B.
Stein leventhal syndrome (polycystic ovary):
-Thick tunica albiginea,  ovarian volume.
-Ammenorrhae, sterility, hirsutism ( androgen.).
-Multiple follicular cysts < 5mm grouped around prephery of ovary.
-Multicystic ovary, if cysts > 5mm + ovarian enlargement.
Teratoma :
-Developmental tumour, arise from totipotent embryonic cells and contain different types of
tissues as bone, cartilage, teeth, hair, brain, thyroid tissue, It may be solid/cystic, benign or malg.
Dermoid cyst is benign cystic teratoma :
-Age: Puberty  menopause.
-Site: ovary, retroperitoneum or pelvic tissue planers.
-Plain x-ray: - Ch. ch. presence of teeth.
- Calcifications.
- Its high fat content makes it radiolucent (is a diagnostic feature when present).
-Us : - Smooth wall, unilocular, cystic.
-Fine strong echogenic internal pattern (fat).
- Contents : mobile & the echoes move with changing position.
- Strong echogenic dental element.(+/-)
- Fat fluid layer may be seen.
-Isotope during thyroid scan:  uptake in ovaries (struma ovarii).

Pseudomyxoma peritonii :
-Entire peritoneal cavity filled with poorly (hypo) echoic. mucinous deposits dt rupture of mucinous
cystadenoma.
Serous cystodenoma :
-Thin wall, hypo or anechoic cyst. may show thin internal septae.
Mucinous cystadenoma :
-The same but contain thick int. septa.
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Cystadeno carcinoma :
- Complex cyst, solid componant, ascites.

Abortion:
-Interruption or termination of pregnancy before age of 28 weeks.
Types :
1. Threatened abortion : Internal os closed.
2. Inevitable abortion : Internal os opened
3. Incomplete : parts of foetus passed & parts retain in the uterus.
4. Complete.
5. Missed .
6. Cervical : stenosed ext. os, prevent expulsion of completely separated ovum.
7. Septic abortion.
8. Therapeutic ,, & criminal abortion.
9. Habitual abortion : condition in which consecutives, spontanesus abortion takes place.
Etiology :
A. Maternal causes :

I. General II. Local causes

i. Acute causes :  fever: measles. 1. Uterine mal-development.
 truma. 2. Truma to body or cx.
 poisoning. 3. Uterine tumour.
4. Cx deep tear, cx incompet.
5. R.V.F.
ii. chronic causes:
- Sp. infection : S, malaria toxoplasma.
- Malnutrition.
- Hormonal dysfunction  pitutiary.
 thyroid.
- Lead poisoming.
- RH. Incompatibility.
B. Paternal cause: (as infertility).
C. Foetal causes:
1. cong. malformation
2. vesicular mole.
3. Placental infarction .
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4. Acute poly hydromines.

Radiologo. Appp: as infertility.

Scrotum and testis:

-Imaging :
I- Plain:  Air  gas forming infection - bowel hernia.
 Calcification : a. Testicular : -Tumour.
-T.B.
-Trauma.
b. Peritesticular  vas deferens  curvi linear in D.M.,B., T.B
 phleboliths in varicocele.
 epididymis  calcif. in cyst wall.
II. US(  5-7.5 MHZ).:
-Indications - Scrotal swelling.
-Scrotal pain.
-Scrotal trauma.
-Subfertility: varicocele – test. atrophy. -Ectopic testis.
Scrotal Swelling:
I. Testicular tumour : 1ry
- 95% are germ cell (origin) rest  mesenchymal, sertoli or leydig cell.
- 25-35 yrs  in undescended testis.
- C/P:  Painless swelling, 10 % bilat.
- U/S: -Seminoma :( most common.)-hypoechoic + ascas of necrosis +
hydrocele.
-Teratoma :- younger age.
-mixed echo  cystic + echogenic areas (bizzare echopatten)
-hydrocele.
- Embryonal cell + Chorio-Carcinoma  highly malig.
-MRI.
-C.T:  paraoartic + para caval LN (at level of renal hilum)
-2ry  from kidney + prostate : -older age.
- leukemia + lymphoma  diffuse hypoechoic.
II. Hydrocele cause : - cong.
- Acq  trauma – tumour.
U/S:  transonic +/- int. echoes in hemato or pyocele.
III. Epididymal cyst, spermatecele.
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Scrotal pain :
1. Epididymoocrchitis :
-Usu. testis not involved - usually dt UTI with: chlamydia, Ecoli, gono, TB, S.
U/S : epididymis : enlarged - hypoechoic + hydrocele + abcess.
Chronic cases  echogenic - thick tunica albuginia.
Isotope.
2. Tumour.
3. Varicocele : more on left  left adenocarc. of kid  renal vein.
Doppler : asses flow. U.S.:
4. Torsion : (U/S changes within 1hr. of onset to save the testis.)
U/S  testis hypoechoic + enlarged.
+/- epid  enlarged.
+/- hydrocele.
Doppler  diff. from epididymoorchitis.
Isotopic  cold area surrounded by activity.

Ectopic tests (  infertility + premalig.)

-Common 70% in inguinal canal. Or high in scrotum - abd. - pelvis.
-U/S + C.T  locate it.
-If not  angio + phelbography.

Investigation of impotence
-Papaverine  v.d ( smooth muscle relaxant)  erection  if not : d.t.  arterial insufficiency .
 venous leak from corpora .
*Doppler : superf. + deep penile arteries.
*Angio:  common + int. iliac then aortic flush angio.
*Cavernosography:  veins  if any dilated veins  ligation.
(N = following papaverine  no veins seen).
*Pharmacocavernosometry  to evaluate venous drainage (inject paprarverine & dilute contrast.
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Obstetrics
-Items:
1. Diagnosis of early preg.
2. Assessment of fetal growth.
3. Fetal positons & presentation.
4. Placenta.
5. Fetal abnormalities.
6. Amount of liquior amnii.
7. Post maturity.
8. Pelivemtery.
9. Fetal death.
10. Ectopic preg.

The role of plain & U/S in pregnancy :

A. Diagnosis of early pregnancy :
-Plain X ray has no role and become historical review .
-U/S : play a major role in detection of pregnancy :
1. The earliest U/S sign of pregnancy is fundal endometrial thickeneing.
2. Abdominal scanning :
i. At 5th wk.:  gastational sac should be visualized as small, well defined cystic
area. & Uterus surrounded by an echogenic rim representing the chorion.
ii. At 6th wk:  embryonic structures apparant  of foetal nodes collection of
echoes  yolk sac & developing amino sac.
iii. At 6.5 wk:  cardiac movement of features identified  crown rump  (from
upper end to lower end = 5mm).
iv. At 8-9 wk:  head, body & limb buds can be seen.
3. Trans-vaginal probe:
i. Gestational sac. : seen as early as 32 days and present in all normal pregnancies.
ii. Yolk sac : seen in 100% of normal pregn. between 36 and 40 days and when the
gestational sac diameter between 6 and 9mm.
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iii. Embryo with a heart beat  in all pregnancies > 40 days when gestational sac >
9mm.

B. Foetal growth :
1. 5-11 weeks: by gestational sac length ( at rate of 0.7-1.75mm/day) 1st trimester.
2. Crown - rump length : from 5-14 w. 1st trimester.
3. foetal femoral length : from 11-22w 2nd trimester.
4. Bi-parital diameter : from 14-38 week. 2nd and 3rd trimester.
5. Head circumference, abd. ciramference.
-Growth retardation :
Def.: 5th centile (%) for weight.
Risk factors :
1. Maternal : hypertension, renal & cardiac diseases.
2. Placental bleeding in early pregnancy.
3. Multiple pregnancy.
4. Previous growth retarded baby.
Types :
Type I :  time onset : 2nd trimester.
 form : symmetrical, the whole body being affected.
 causes:( foetal): - Genetic.
- Chromosomal abnormalities.
- Malformation., I.U. infection.
- Drugs : alcohol, smoking.
Type II :  time of onset : 3rd trimester.
 form: asymmetrical, the trunk being affected > head   H.C/A.C
ratio (head/abd) trunk smaller < head
 causes (maternal & placental):  Hypertension.
- Renal vascular disease.
- Placental insufficiency.
- Idiopathic.
C. Foetal position and presentation :
- Lie : relation of long axis of foetus to that of mother  longit.
- Presentation : the part of foetus lying lower  vertex.
- Attitude : relation of different parts of foetus to one another  flexion.
- Position : relation of back of foetus to ant. abd. wall  Lt. ant. occipit.
- Any abnormality of the lie, presentation & attitude , should arouse suspicious of
abnormality of the mother & the foetus:
 Maternal causes :
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- Ovarian dermoid.
- Uterine fibroid.
- Abnormalities of pelvis.
 Foetal :
- Placenta previa, hydrops.
- Polyhydromnios, multiple pregnancies.
- Foetal death .
D. Placental development and abnromalities :
1. Normal placnetal development :
The placenta can be identified at about 8ws as a granular thickening of gest sac.
a. Entire surface of placenta is covered with villi  implantation ot 6-7 w. (Gest.
age week).
b. Villous placenta (chorion frondosum) develop  7-11 w.
c. Atrophy of remaining villi (chorion laeve)  7-11 w.
d. Three layers of placenta identify  12w.
-Basal plate. -Placent. substance. -Chorionic plate.
2. Placental grading :
- The normal placenta show U/S feature which change as the pregnancy progresses:
O homogenous + no + no + no
I echogenic (scattered) + no + no
II echogenic (comma) + calcificaties + demarcated cotyledons
III all + echo poor areas (central)

Changes in 3 zones Grannum classification

Basal layer placent. substance choronic plate

Grade O No densities ie Finely Straight & well
no calcification homogenous defined
Grade I No densities few scattered subtle undulation
echogeneic areas
GrII Linear Echo-densities Demarction of
arrangement of comma shape cotyledons (endo)
small echo- directed to basal
densitis layer
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Grade III Larger & partially Circular densites  septation of
confluent with central echo- cotyledons,
echogenic areas poor areas  extending to the
villous spaces for basal layer
blood
transportation

3. Placenta and membranes in twin pregnancies:

1-Dichorionic Diamniotic (single placenta).
2-Dichorionic Diamniotic (separate placenta).
3-Monochorionic Diamniotic.
4-Monochorionic Monoamniotic.

4. Abnormalities of the placenta:

Placenta preavia:
-Def.: A portion of placneta covers the internal cervical os.
-Incidence :
U/S:  20% at 20 weeks gest. (termed low laying, if it does not completely
& symmetrically cover os).
 0.5% at term. (due to differential growth of the uterus and develop.
of the lower ut. segment).
-Predisposing factors : -Maternal age.
- Multiparity.
- Previous uterine surgery.
Classification:
- Type I (minor)  low laying plac.:
The placental margins, extends into lower segament but does not reach internal os.
- Type II (marginal):
The placental margins, extends into the lower segam. as far as margin of internal os.
- Type III:(Asymmetrical Complete):
The placenta covers the internal os, when it is closed.
- Type IV:( symmetrical Complete):
The placenta cover the internal or, when it is partially or fully opened.
The firm diagnosis of placenta praevia should not be made before 32 weeks as the
change relation ship of placental margin to internal os}.

Association = complications:
1. Maternal Hge (APH).
2. Abnormal presentation.
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3. I.U growth retardation.
4. Preterm delivery.
5.  pre-natal mortility.
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Placental hge :
1. Retro-placental hge : concealed ante part hge.  separation of placenta.
2. Marginal Hg .  separation of placenta.
3. Pre-placental Hge : either subamniotic or subchorionic.
4. Intra-villous thrombosis  intra-placental sons lucencies.

Placental Abruption :
Premature separation of normally sited placenta either : marginal or retro-placental.

Cause of a thickened placenta > 4 cm:

1. D.M. 2. Foetal hydrops 3. Intra-uterine infection.

Cause of thin placenta :  intra-uterine growth retardation.

Gestationl trophoblastic disease :

Types :
1. Hydatidiform mole. 2. Invasive mole.
3. Chorio- carcinoma.
-U/S : 1. Large echogenic mass, occupying the uterine cavity with numerous
small fluid-filled spaces < 15mm classically seen in 2nd trimester.
2. No foetal parts except in partial mole.
-Chest x ray  choriocarcinoma : (snow storm metastases).

N.B.First trimester -Abnromal gastational sac :

Abd US :
Major criteria :-large gastational sac > 20 mm without yolk sac.
-distorted gast. sac shape.
Minor criteria :-thin decidua < 2mm.
-weak decidual amplitude.
-Abscent double decidual sac sign.
-low position.
Endovaginal US : -Gast. sac > 20 mm without yolk sac.
-Or gast sac > 16mm without an embryo.
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E. Foetal abnormalities:
1. Foetal death :
-C/P : absent foetal movement.
- Plain x-ray findinges:
a. Spalding sign :- over riding of the cranial bone.
-evident between 5-15 day after death.
b. Gas translucenies : seen in blood vessels of chest, Abd, & heart
- transient for 12 hrs. only.
c. Attitude of extreme flexion 5-15 day after death.
d. Devel’s halo sign : elevation of peri-canial fat by underlying
soft tissue oedema.
- appear within 2 days after death.
e. failure to grow on serial films.
f. Disparity between clinical & radiolog. estimation of maturity.
g. Constancy of foetal postion.
- U/S findings :
1. The vital sign of foetal movement & cardiac pulsation are
absent.
2. Other delayed signs  U/S spalding sing, halo sign.
3. Abnormal gastational sac (early in 1st trimester).

2. Extra-uterine pregnancies (ectopic):

- Plain x-ray :
1. Unusual : lie, attitude (swiming), position high, low in abdom).
2. Constancy of foetal attitude, position on repeated examination.
3. In lateral view  foetus may overlape maternal spine or closed
to maternal abd. wall.
4. Unusual clarity of the foetus.
5. Absence of shadow of uterus.
6. Abdominal gas of mother overlie the foetus.
- U/S :
1.U/S evidence of an intra-uterine pregnancy exlude the
diagnosis.
2. Endo-metrial thickening (decidual cast), pseudo-gest sac.
3. Adenexal mass (complex echogenic mass).
4. Fluid in Douglas pouch.
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5. Demonst. of living foetus outside the uterus.

6. HCG level > 1800 M.I.U / ml. with no evidence of an intra-
uterine pregnancy.

N.B . Absence of I.U pregnancy with +ve pregnancy test :

a. early preg. b. ectopic. c. recent complete abortion.

3. Multiple pregnancies :
- Plain : - conjoined twins :
 constancy of position between foetuses.
 deflexion of both foetal spine.
- Growth discripancy between them = death of one of them.
- Easy recognition of two foetus.
- U/S :
-For placenta.
-Easy recognition of two foetus.

4. Abnormal quanitity of liquor amnii:

- Poly hydramnios :
Plain:  disportion between size of uterus & foetus
- Unusual attitude.
- Unusual unclearity of foetus.
- Oligo hydromnios :
 un usual clarity of foetus
- U/S :
Liquor volume :
It increase in normal pregnancy until 34-40 week, then decreased
(400ml at 20w).
Assessment of liquor volume is usually subjective. but < 2 cm
pools in any direction indicate its reduction (four quadrants).
Causes of polyhydraminos:
1. D.M.
2. Fetal anomaly:  hydrops.
 heart failure.
 diaphrag. hernia.
 T.O.F, duodenal atresia.
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Causes of oligohydromnios :
A. Severe :
1. Renal agenesis. 2. Premature rupt. of memb.
3. Sever growth retardation.
B. moderate :
1. Bilat renal anomalies.
2,3. as above.

5. Congenital abnromalities of foetus:

A. Hydrops foetalis:
Def. Excessive fluid accumulation in the extra-vascular component :
= s.c. oedema + ascitis, pl. & peric effusion.
Types :
1. Immune hydrops:
 Rh. Incompatibility.
 Blood group abnromality.
2. Non-immune : late manifest. of many sever diseases.
Plain X-ray :
- Attitude  Buddha.
- Elevation of peri-cranial fat : Halo sign.
U.S.
B.Thyroid, cystic hygroma :
- Soft tissue mass of neck  extension of neck  face or brow
presentation
C. Renal :
- Hydro-nephrosis.
- Multcystic kid.
- Poly-cystic kid.
D. CN.S:
1. Anencephally : the cranial vault fail to develop and bone of skull base,
face are maldeveloped.
2. Micro-cephally :  facio-cranial disproportion.
3. Hydrocephalus : usually associated with spina bifida.
-U/S : - distended lateral ventricle.
- head size : B.P.D & H.C.
4- Spina bifida: - Failure of fusion of post neural arch. at 3-4 weeks.
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-It may be open or closed by membrane.

- Meningocele only CSF in present in sac.
- Myelomeningeocele : commoner.
- Lumbosarcal region : 90%.
- Abnormalities of fetal cranial contour (lemon sign) & of the cerebellum
(banana sign).
5. Arnold-Chiari malformation.
D. Anterior abd wall defect :
1. Gastro schisis (malrotation of intestine).
2. Exomphalos  abd. wall defect due to failure of S.I. to re-enter the
abdomen.
E. Cong. diaphragmatic hernia:
U/S: - Displaced heart.
- Bowel in thorax.
- Polyhydramnios
F.Cardiac abnormalities.
G. Skeletal dysplasia:
Depend on  abnormal bone growth for gestational age.
H. Development of limb :
i. Symmelia : fusion of limb in whole or in part.
ii. Amelia : absence of limb.
iii. Hemimelia : absence of distal segam. of a limb.
iv. Phocomelia : absence of proximal segam. of limb.

F. Post maturity :
-Def. peristence of foetus more than 42 weeks of gestation.
-Etiology :
1. Hereditary.
2. Hormonal due to  estrogen &  progesterone
3. Non engagement of presenting part due to disproportion, mal-
presentation, floating presenting part or anecephaly.
4. Wrong date.
-Radiolog. features :
A. Plain x-ray :
1. Excessive length of foetus (> 52cm).
2. Over sized foetus (occasional normal).
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3. The bones of skull are hard, thick & suture lines and fontanels
are narrowed or closed.
4. Appearance of an ossification center in cuboid bone at birth.
5. Presence of large ossif. c. in upper end tibia and lower end
femur (normally at birth 36-40 w).
6. Distorted pelvic cavity.
7. Malpresentation : breech, brow.
B. U/S :
1. Change in placenta  grade III.
 degeneration of placenta or separation.
 calcifciation.
2. Marked  in amount of liquor (turbid).
3. Measurement of foetus : B.P.D, H.C.:, A.C :all are above of 42 weeks.
4. Signs of predisposing factors e.g. malpresent, anencephaly.
5. Signs of distress of the foetus.
G. Pelvi-metry :
-Clinical indication:
1. Persistent breach presentation.
2. Following difficulties of the previous labour.
3. Post-maturity.
4. Failure of head engagement after 36th w.
5. Suspected pelvic deformity : old rachitic female.
-Obstetric feature of pelvis.
1. Gynagecoid pelvis : -optimum round pelvic brim.
-max. trans. diameter is anterior.
2. Android pelvis (male): - max. trans. diameter is displaced posterior.
3. Anthropoid : - oval conjugate > trans diameter.
4. Plate pelloid : - brood or flat trans > cong.
- Abnromal pelvis :
A. Congenital :
i. Achondroplasia  conjugate line.
 lordosis.
ii. Nagel pelvis  aplasia of one sacral ala  asymm. pelvis.
iii. Robert pelvis  both sacral ala fail to develop.
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B. Acquired :
1. Traumatic  pelvic deformity.
2. Metabolic disease  rickets, osteo malacia  bone softening
 weight bearing  tri-radiate pelvis.
3. Spondylolisthesis.
4. Hip disease : septic or T.B., dislocation.
5. Polyomyelitis.
6. T.B or osteomylitis of the spine.
-Radiographic technique :
The measurement taken on the film are subjected to geometric enlargement which
must be reduced by an appropriate correction factor :

Distance of appropriate plane of pelvis from focal spot

___________________________________________
Focal film distance.

Technique:  Erect lat. View.

 Supine A.P view of the pelvis.
Pelvimetry :
1. True conjugate line  11cm. from sacral promontory to sup. and post.
part of body of s. pubis.( Lat/erect).
2. Pubo sacral line  11.5 cm, from lower most fipart sacrum to inferior
& post of body (lat/erect).
3. Transverse D  12.5 cm from widest diameter of pelvis.(AP / supine)
4. Inter-spinous : 10cm between two spinous processes( AP / supine).

U/S:-Indications for U/S in first trimester :

1. Threatened abortion.
2. Suspected ectopic preg.
3. Uncertain L.M.P.
4. Evaluation of retained products post spontaneous abortion.
5. Assessment of success of ovulation induction.
6. Retained I.U.D.
7. Evaluation of pelvic mass in early pregnancy.
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U/S findings in threatened abortion :

1. Intact pregnancy in 50%.
2. Blighted ovum 25% .
3. Missed abortion.
4. Incomplet abortion.
5. Ectopic.
6. Hydatidiform mole.

Blighted ovum :
-A fertilized ovum in which development had been arrested.
-U/S  of an empty sac :  No foetal parts seen in ! sac.
 No yolk sac with !sac > 20 mm.
 Irregular sac contour.
Normal uterus :
-Nullip post pubertal 7 x 4 x 5 cm (Length x depth x width).
-Multiparity :  in uterine size 1cm in all direction.
-Post-menopausal : 3 x 2 x 2cm.
-Endometrial thickening : i. Proliferative phase = 3-5 mm.
ii. Secretory phase = 5-6mm.
(Seen as a thin continuous line).
Normal ovary :
Ovulation : occurs at a follicular size of 20-24 mm in normal cycles.
U/S signs of ovulation :
1. Collapse of follicle.
2. Free fluid in D.pouch.
3. Echo free zone around endometrium.
N.B. :
1. Developing follicle  0.4-1.4 cm.
2. Mature follicle  1.5-3cm.
3. Follicular cyst  > 3cm.
H.S.G:
-Indications :
1. Demonstration of tubal patency.
2. Cong. anomalies, of ut. & cx.
3. Abortion (habitual abortion).
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-Contraindication :
1. Pregnancy.
2. Acute pelvic infection.
3. Week, before and after menstruation.
4. Severe, cardiac and renal disease.
5. Sensitivity to C.M.

-N.B. : Asherman’s syndrome :

Adhesions or absence of uterine canal following delivery, pregnancy or curettage.
U/S : - May shows normal shaped uterus with no cavity.
- Haemotosalpinx or haematometra.

Ovarian masses:
A. Simple cystic structures :
1. Follicular cyst.
2. Cyst adenoma.
3. Polycystic ovaries (multiple, 5-8 mm in diameter, echogenic stroma).
4. Cystic teratoma.
B. Complex (mainly cystic):
1. Cystadeno carcinoma.
2. Dermoid.
3. Abcess
4. Ectopic preg.
5. Endometriosis (chocolate cyst).
C. Complex (mainly solid):
1. Cyst adeno-carcinoma.
2. Dermoid.
3. Ectopic preg.
D. Solid :
1. Adeno -carcinoma.
2. Solid teratoma .
3. Fibroma.
4. Lymhoma.
5. Metastasis .
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Breast:
Anatomy :
1- Functional element (parenchyma ducts and alveoli).
2- supportive element: (stroma fat loose CT dense c.t).
N.B. Most of the glandular tissue are located at the upper outer quadrant that is
most of the tumor are seen at that site .

Radilogical and pararadiological methods of examintion of the breast:

A. Mammography :-
Technique: is based on principles of soft tissue film these are :-
1- Low K-V (soft film ).
2-High M-A-S (to compensate low K-V- for adequate exposure).
3-Collimating beam (to decrease the scattering radiation ).
4- Small focal spot ( to decrease geometrical blur).
5- Short object film distance (to decrease geometrical blur).
6- Non screen film to give the maximum details (decrease scattering).
7- Compression of breast to ↓ thickness & movement (decrease blur)

Views: - Basic : (cranio-caudal, mediolateral).

-Accessory :(lateral oblique = axillary view ).
Indication:
1- Symptomatic female eg eczema, nodular breast.
2- As screening for Asymptomatic females above 40 years.
3- Examination of bereat in a female with cancer on the other side.
4- Guided biopsy (plate -wire technique ):
-By using plate on mammograph locate exact position of lump then introduce wire
in the same site (determined by both views .)
-The surgery takes biopsy guided by the wire inside, then takes another film after
taking biopsy to be sure of correct technique.

B. ULTASOUND:
- Using real time scanning 5 or 7.5 Mhz transducers.
- Using linear transducer with water bag.
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INDICATION :
1 - Differentiate cystic from solid lesions .
2. Dense breast (dense parenchyma mainly in pregnant and lactating ).
3- Tendre breast (compression for mammography is not possible )
4- Non palpable opacity seen on mammography.
5 - Palpable lump with negative mammographic findings .
6- Fine needle biopsy guided by ultrasound.

DISADVANTAGE:
1- Fine microcalicification can not be detected.
2- Tumor < 1cm can not be demonstrated .
3- Colloid carcinoma give similar picture as benign lesions.

C. Galactography :
-Indication : Blood stained nipple discharge .
-Technique : Blunt needle into nipple select duct inject contrast (urographin)
films see opacified ducts.
-Data : 1- Course: -Regular.
-Amputation = duct carcinoma.
2- Calibre (up to 2mm): - Smooth dilatation (pregnancy and lactation ).
- Irregular narrowing with distal dilatation
invasive ductal carcinoma .
3-Filling defects (in the duct): - Smooth : papilloma, granuloma .
- Irregular: invasive intraductal carcinoma
D. Thermography:
Non specific to demonstrate thermal and vascular abnormality in different
breast lesions  infection (abcess).
 malig.

E. Computed tomomogaphy :
Its main side effects (high dose of irradiation )
- Cysts: appears as well defined low density area.
- Solid mass : appeares as homogenous area of high density (soft tissue density ).
- Detection of axillary and internal mammary lymph nodes.
- Enhanced scans 60 H.U  suggests malignancy .
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F. MRI:
High sensitive method with no inoizing radiation.
Limitations:
1- Economic factor. will be solved
2- Time consuming ( take I hour). will be solved
3- Uncomfortable for patient. as in CT.
4- Can not detect microcalfications. O.K.

G. Xero-mammograghy:
- High dose of radiation.
- Using selenium plates.
-+ ve and -ve zerogram.

H. Digital mammography:
- Using the already taken views  scanned by laser scanner →into computer
manipulated and contrast alteration.
- Using phosphrelation plates instead of the film  laser scanner ,,,,
- Using digital detectors direcly into computer.

N.B. BENIGN LESIONS:

Density margin &calcification

Fiberoadenosis
Fibroadenoma similar to breast or ↑if partially ill defined+smooth
large calcification, central or
periph.
Cyst more dense egg shell calc
Lipoma ↓density
Fat necrosis ↓density egg shell
Galactocele ↓density egg shell
Abscess ill defined
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MAMMOGRAPHY:
Normal mammographic patterns:
1- Adolescent pattern: young girls -Less fatty element (less stroma).
- Dense glandular disc, clearly separated from subcutaneous fat
- Ducts, vessels and trabeculae are not identified  difficult diagnosis of the mass. ----
- Clear retro mammary fat.
2- Mature glandular pattern:
- Adult females, especially after repeated pregnancies
- Fat amount increased within glandular portion so more definite structures - as
ducts vessels.
3- Fatty atrophic pattern:
-Perimenopausal female ,fertile, multipara.
-Excess fat replacing the glandular portion  good demonstration of the pervious
structures, also lactiferous ducts may be seen.
-Better demonstration of masses and calcification.

MAMMOGRAPHIC DATA:
A-MASS :
sign Benign Malignant
1 Density less than malig increased density
2 Texture homogenous heterogenous
3 Margin regular irregular comet tail +stellate
4 Speculation -ve + ve
5 Lucent halo found +/-
6 Size clinically = radioloqy clin> radiology
B- calcification:
1-Microcalcification = Malignant.
-0.08 -0.1 mm.
- Granular / elongated with irregular outline.
- Commonest in scirrhous carcinoma - usually occurs in clusters = > 5 in
tumour or outside (punch like).
2- Macrocalcification coarse = Benign.
A- regular and smooth:
-Ring /tubular along ducts  duct ectasia.
surrounding a transradient center
- Pop-corn  fibroadenoma.
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- Egg shell - > cyst, galactocele, fat necrosis.

- In amorphus lump - > scar and fat necrosis ( mottled).
- Punctate - > papillomatous or post radiotherapy.

C- secondary signs( breast architecture):

Sign Benign Malignant

1 skin no skin dimpling retracted dimpled thickened
2 nipple no retraction retracted
3 fat no obliteration obliterated
4 parenchymal compressed destroyed
pattern
5 ducts +/- dilated dilated
6 vascularity + ve only with infam increased
7 L.NS +ve only with inflam ++ ve LN. enlargement
8 perifocal no yes
haziness

Fibroadenoma:
-Well defined contour all around.
-Halo translucency around (capsule).
-Homogeneous, Small, No skin or deep attachment.
-Pop-corn calcification.

Malignant lesion:
- Nipple retraction.
- Skin dimple, thick.
-Ill-defined mass.
- Micro calcification.
- Stellate fibrous bands.
- Cooper lig. Involvement.
- Hazy scalloped contour.
-Commit sign (orbit cone). Mostly scirrhous.
N.B.:-Signs of malig .without definite mass……?? Paget dis.
-Worst is mass in an already dense breast (glandular or cystic)&also in ! upper
medial quadrant (not seen easily in the film).
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X-ray and U/S in breast lesion:

Disease X ray mammography Ultrasonography

1. Cyst. Single or multiple Anechoic
Types: Well defined density Well defined
-Simple. Shape: smooth border Rounded or oval
-Thick content. +/- lucent rim of fat (halo) Post acoustic enhancement
-Hemorrahgic. DD (fibroadenoma Surrounding tissue is (normal or
-Infected. compressed)
-Sebaceous. Special
-Multiple. Thick content  fine echos
Infected  irregular hazy lesion
with mild echogenicity
Hgic  dense internal echoes
2. Abscess. Like cyst If acute  as infected with loss of
echo free texture of subcutaneous
fat.
Chronic = +/- illdefined
heterogenous echos
3. Lipoma. Usually large, rounded, Well defined hypoechoic
radiolucent, compression of No post acoustic enhancment
surrounding tissue
4.Fibroadenoma Dense rounded or lobulated Smooth, well defined, round or
-most common Surrounding lucency halo oval
-Young adult Pop-corn calcification - Low level homogenous internal
-Uni/bilateral Ductal proliferation (tubular echos
lucency) Hypoechollic or iso or hyper acc
DD to adenosis & fibrosis.
Cystosarcoma phylloides Ductal proliferation
(non homogenous) If, calcification  post acoustic
shadowing
Only breast architecture distortion
may be the sign
5. Mammary dysplasia Well defined 1. Pleomorophic echopattern
-Common Mixed density fibrotic = echogenic
-Cystic (fibrotic, cystic, glandular) Cyst = hypoechoic
formation Ductal proliferation Gland = hypoechoic
-Epithelial Ducts = serpigenous
Proliferation Tubular echoes
-Premalig. 2. Fibroglandular
3. Decreased subcut fat and
increased fibrosis
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6. Carcinoma as before, mass, calcification 2ry 1. Hypoechoic mass with irregular

-Scirrhous Medullary signs outline
2. Heterogenous internal echos
3. Surrounding hyperechoic hallos
dt odema
4. Postacoustic shadowing
5. S.C. fat invaded dense echos
with thick coopers ligament
6. Skin thick bulging.
7. Axillary L.Ns enlarged
Calcified  dense echos
CT :  mass  mucocele, +ve
contrast
 extension  axilla LN,
Mediast LN, Int mammary.

MRI :
1- Abcess – T1  low center + high capsule .
- T2 Strong enhance.
2- Fibroadenosis  cysts : low T1 – high T2 – Not enhance.
 diffuse + delayed enhancement in proliferative type.
3- Fibro adenoma : low signal
post contrast  very strong (Myxoid 40 %, not enhance (= fibrous).
4- Papilloma  enhance expect sclerosed (solitary + subareolar  Benign.)
(multiple  Malignant).
5- Lipoma  not enhance, high on T1.
6- Cancer  fast + focal enhancement .
> 83 %, 60 sec. Post contrast.

Foot & Stewert classfication of cancer breast :

(1) Paget disease of nipple 1 %
(2) Cancer of mammary ducts :
- Non inf. papillary, comedo.
- infiltrating  papillary, comedo.
 Adeno - Scirrhous 63 %, atrophic.
 Medullary = Encephaloid = Anaplastic.
(3) Cancer of mammary lobules –> non inf.( = CIS) & infiltrating.
(4) Rare : Mastitis carcinomatosis & Colloid carcinoma..
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Staging of Cancer breast :

TIS Carcinoma in situ.
T1 tumour < 2 cm.
T2 tumour 2 – 5 cm.
T3 tumour > 5 cm < 10 cm + skin infiltration and pectoral fixation.
T4 tumour > 10 cm.
No no.
N1 Axillary mobile.
N2 Axillary fixed.
N3 Supra clavicular.
Mo no.
M1 Metastases.

FIBROADENOSIS:
Age: child bearing period.
CIP: periodic mastalgia related to menstrual cycle - palpable nodularity - tenderness
of breast tissue.
RADIOLOGICAL APPEARANCE (mammography):
 Mass:
-Similar density as breast tissue except if large density.
- Margin : smooth rounded ovoid or lobular.
but m.b partly irregular or ill - defined as they develop form surrounding
fibroadenoid tissue.
-+/-Cysts  prominent ducts.
 Calcification :
-Smooth calcification central or peripheral .
 Changes in breast architecture:
- Architecture is deformed by mass.
- Halo around ! lesion d.t. compressed fat.
- Prominent ducts.
 Vascularity :.
 no Perifocal haziness.
 Size of lesion = or > clinical size.
U/S:
Small ,well-defined with uniform internal echoes - dense echoes of int. calcification
(u/s: fat hyperechoic but in breast hypoechoic and glands are hyperechoic).
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Thyroid Swellings
CAUSES :
1-Simple nodular goiter(Diffuse or nodular).
(Goitre =thyroid enlargement, non neop ,non inflam).
2- Toxic goiter :( Graves dis. Or nodular).
3- Malignant goitre.
4- Thyroiditis: acute, subacute, ch. (Hashimoto).

INVESTIGATIONS:
1) Plain x ray film of the neck and thoracic inlent:
1- Soft tissue mass in the region of the thyroid gland.
2- Retrosternal extension  ant mediastinal mass.
3- Retrotracheal goitre (posterior displacement of the esophagus and anterior
displacement of the trachea).
4- Calcification (amorphous = maligant) and (well defind= benign).
5- Metastatic deposits (cancer deposits -> miliary secondaries).

2) U/S:
Using linear transducer 7-5 MHZ with water bag (Diff .cyst or solid, measurement)
1- Colloid multinodular qoiter:
- Hypoechoic nodules with foci of echogeninty (fibrosis .)
- Small cysts within and in between nodules.
2- Thyroid adenoma:
- Hyperechoic lesion surrounded by a smooth halo around the lesion.
- Central cystic areas (hypoechoic).
- Areas of fibrosis and calcification (hyperechoic ).
3- thyroid cysts:-
-Well defined , thin wall anechoic with distal enhancement .
-Due to degenerative changes or hge in colloid goitre or in malignant nodule
4- Thyroid carcinoma: -Papillary cervical L.N.
-Follicular  blood metastasis
-Anaplastic-> occurs in old age
*hypoechoic = poor enchogenic mass , invading the thyroid capsule and tissue.
*Fine Needle Aspiration Biopsy is diagnostic.
5- Hashimoto: -coarse paenchymal pattern d.t. lymphatic infilt + small nodules
with scarring, cyst and calcification.
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3)Computed tomography:
-Can differentiate between thyroid and parathyroid tumors .
-LN. -Extension.

4) Isotope study : (I131 or T.C 99 m )

- Nodule  hot = toxic
 cold = Malignant or
Benign (cyst, focal thyroiditis, degenerative) U/S
- Retrosternal goiter activity is below sternal notch .

5) M.R.I.:
- Clear demonstration of thyroid mass and retrosternal extension with coronal and
sagittal scans .

PHARYNX AND LARYNX:

Nasopharyngeal lesions :
A- Developmental lesions:
1- Meningoceles:
- Rare, usually associated with a defect in skull base.
-Seen in coronal sections of C.T.
2- Choanal atresia:
-Instillation of lipidol into nostril followed by films in the lateral and base
projections  give an accurate outine of the atretic septum .
3- Adenoids : (Important)
-Lat. Film: -Size of adenoid pad.
-Width of postnasal space airway.
4- Antrochoanal polyps:
- Lateral film smooth pear-shaped soft tissue mass in the postnasal space.
- Associated with complete or partial opacity of antrum.
- NO bone erosion.
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B- Benign tumours:
1) Juvenile naso pharyngeal angioflbroma:
-The commonest benign tumor of the nasopharynx.
- In pubescent males.
C/P: -Epistaxis and nasal obstruction.
-Dark red mass in the nasal cavities and post nasal space.
C.T:
1- The mass arise at or close to the base of pterygoid lamina .
2- Bone erosion in this site (constant feature ).
3- Expanding into the nose and post nasal space .
4- Tendency to spread laterally through pterygo-maxillary fissure 
A- widening of the fissure.
B- Extension into the infratemporal fossa.
5- Anterior : bowing of the posterior wall of the antrum (important sign ).
6- Involvement of orbit  proptosis (late.).
7- Coronal cuts  extension into sphenoid sinus and cranium .
8- Post-contrast studies (bolus):
A- Considerable contrast enhancement .
B- Help to delineate limit of lateral extension in infratemporal fossa.
CAROTID ANGIO:
- Not necessary but diagnostic .
- Its main value is embolization to reduce blood to the tumour prior to the surgery or
to stop severe epistaxis

2-CHORDOMAS (locally malig) :

-Midline tumors occurring in old age from primitive notochord.
C.T:. -Large soft tissue mass in the post nasl space.
-Destruction of the basisphenoid (clivus )
± Calcification .
- Usually associated with intracranial mass.

C- Malignant tumours:
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1- Sq cell c. (nasopharyngeal carcinoma):

Presentation :
1-Large soft tissue mass in the post nasal space.
2- Direct infilteration through the skull base  cranial nerve lesion.
3- Lymphtaic spread  enlarged cerv.L.N.
4- Malignant otitis media and deafness result from obst. of eustachian tubes .
Skull base view:
Erosion of the bone of middle cranial fossa and atlanto occipital region .
C.T( high resolution) :
1- Erosion.
2- Oblitration of the lateral pharyngeal recess (fossa of Rosenmuller ).
3- Obliteration of the soft tissues planes + Cervical L.N.

2- Lymphoma:
Bulky tumor without early invasion of the parapharyngeal spaces.

DD of mass in nasopharynx:
-Cong: adenoids, meningcocele.
-Trauma: fractures haematoma.
- Inflam: infection  gas in the mass .
- Neoplasm.

PHARYNGEAL AND IARYNGEAL LESIONS:

(stridor, hoarsness, dysphagia, lung abscess)
1- Functional disorders:
-Cricopharyngeal dysfunction (appears in cineradiology)
2-Traumatic lesions:
-FB ( fish or meat bones, coins, pins ) lodged in the upper oesophagus, pyriform
fossa, between the cords - perforation by F.B or instrumentation widening of
the retropharyngeal soft tissue space (haematoma).
3- Infection: Retropharyngeal abscess.
4- Laryngoceles:
-An air filled sac arising from laryngeal ventricle and saccule:
1- Congenital.
2-Acquired (expiration against resistance ) e.g. - glass blowers.
- trumpeters.
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-Either: - Internal (lie inside the thyroid lamina ).

- External (lie outside the thyroid lamina soft tissue mass).

-Investigation:
1-AP and lat views the neck with forced expiration.
2- C.T demonstration of small laryngocele.
3-Tomography (AP) demonstration of small laryngocele.
5- Tumors of the pharynx:
1- Malignant tumour of the oro and hypopharynx:
-Radiologically :
a- Soft tissue mass enchroaching on normal air filled spaces
vallecula or pyriform fossa.
b- Filling defect in Ba swallow.
c- Changes in mucosal relief pattern .

POST CRICOID CARCINOMA:

-Sq.cell .C.
-PDF web plummer vinson syndrome.
-Radiolog :
1-Widening of the  post cricoid space  1cm (normally wide in child.)
2- Irregularity and hold up in Ba swallow + spill over trachea.
3- Destructed mucosa , irreg outline of pharynx.

Tumours of the larynx:

1)Benign tumours of the larynx:

A- papilloma: (sq cel)
- common in adult.
- pre–malignant.
- usually single may be sessile or polypoid.
(in child multiple  recurrent resp. distress).
B- Chondroma: arise from one of the larygneal cartilages+ speckled calcification.
C- Plasma cytoma : smooth rounded tumor of homogenous consistency (=localized
multiple myeloma ) the larynx is the commonest extra medullary site.
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2)MALIGNANT TUMOURS OF THE LARYNX:

A-Glottic tumour
-Carcinoma of the true cords is commonest form of intralaryngeal growth 
fungating mass in lat. view neck.
-Present early with hoarseness
-CT:
-At this level the thyroid laminae, arytenoid cartilages and the cricoid lamina are seen.
*paraglottic space: between the mucosa and cartilage seen as a translucent line
just deep to the thyroid lamina (absence of the line indicate tumor infiltration).
*Ant. Commissure: seen as a free space consisting of mucosa lying directly on
cartilage in midline between the anterior attachment of the cords to thyroid cartliage.
*Arytenoid cartilage: small, homogeneously calcified triangular structure lying
anterolateral to cricoid lamina .
(Involvement of the thyroid arytenoid cartilages or suglottic spread = worse prognosis)

B- Supraglottic tumours :
-Growths arising from vallecula or in the ventricle.
-Best assessed by endoscopy.
- Plain: raged appearance of the epiglottis due to edema.
-Computed tomography :
- Demonstrating invasion of the base of tongue (may be infiltrated ).
- Obliteration of the ventricle.
- Erosion of the thyroid cartilage and thyroid gland .

C- Sub-glottic tumor:
-Least common (best by CT ).
-Arise from undersurface of the cord  subsequent cord involvement.
-Difficult to assess by endoscopy (hardly seen).
-C.T. Value:
1- Invasion of cartilaginous skeleton of larynx by tumor  Asymetry,
immobility due to tumor.
2- Gross involvement of thyroid laminae.
3- Ossification of arytenoid, cricoid, thyroid lamina.
-Tommography showing :
A- Asymmetry.
B-Immobility of the cord results form infiltration or paralysis of the R.L.N.
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Lesions of the infratemporal fossa and parapharyngeal regtion:

1- Carotid sheath tumour: 1-Glomus jugular tumour.

2- Carotid body tumour
3- Neurognic tumour (neuoma).
(Typically they sepaerate carotid a. and jugular v.)
2- Lipoma & Teratoma : Low density of fat content is suggestive of the origin.
3- Meningioma : Extending form skull base.
4- Salivary tumours: - Arising within the pharynx.
- cleavage plane can be seen between the parotid gland (salivary adenoma)
- obliteration of fascial planes in malignant tumours.
5- Enlarged L.N.: -Bolus injection  nodal rim enhancement
INVESTIGATION:
1- C.T value:
a-Axial : position and extent of the tumour.
b- Coronal : Extension of the base of the skull.
c- Bolus ( shows the degree of enhancement, position of major vessels )
2- Parotid sialogram: relation of the mass to ! deep lobe .

ACUTE UPPER AIR WAY OBSTRUCTION:

-Most common in infants due to small calibre of airways.
-Causes:
1- Choanal atresia (how acute):
Bilateral or unilateral / bony (90%) or membranous/complete or incomplete.
2- Laryngo tracheobronchitis: narrowing of glottic and subglottic regions by
inflammatory edema.
3- Acute epiglottitis:
a - Swelling of epiglottis, aryepiglottic, folds, uvula & prevertebral soft tissues.
b- Hypopharynx and pyriform sinuses are distended with air .
4- Retropharyngeal abscess :
- widening of the prevertebral soft tissue.
-  gas or air fluid level.
5- Angio- oedema: - due to allergic inhalation of noxious gases
6- Foreign body: (Important).
7- Retropharyngeal hge: trauma, neck surgery, direct carotid angioraphy shows
widening of the retropharyngeal soft tissue enlargement.
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CHRONIC UPPER AIR WAY OBSTRUCTION:

A - Child :
1- Nasal : 1-Choanal atresia.
2- Nasal angiofibroma.
3- Antrochoanal polyp.
2-Supraglottic : 1- Grossly enlarged tonsils and adenoids.
2- Laryngomalacia.
3- Cysts of the epiglottis.
3-Glottic : 1- Laryngeal polyp.
2- Papilloma.
4- Subglottic and trachea :
1- Tracheomalacia (weakness of the tracheal wall)
-Primary : (premature infants).
-Secondary :
A. Tracheo Oesophageal Fistula.
B. Vascular ring.
C. External compression by tumour.
D. Prolonged tracheal intubation.
2- Subglottic haemangioma.
3- External compression by (L.N., thymic enlargement)

B- Adults :
1-Supraglottic : -Carcinoma of larynx.
2-Glottic : 1- Carcinoma of the glottis.
2- Vocal cord paralysis ( after thyroidectomy ) bilateral.
3-Subqlottic and tracheal:
1-Extrinsic compression (L.N, local invasion by carcinoma of bronchus, thyroid
and oesophagus )
2- Infraglottic carcinoma.
3- Tracheomalacia due to prolonged tracheal intubation…. etc.
4- Tracheal malignancy : (sq. cell carcinoma).
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*Causes of widening of the lower cervcial prevertabral space:

1- Pharyngeal abscess & diverticulum.
2- Pott’s disease.
3- Thyroid, parathyroid tumors.
4- Post cricoid carcinoma.
5- Lesions arising from the spine.
6- F.B edema of the prevertebral space or hematoma.

Paranasal sinuses:

Acute sunusitis :
 Thick mucosa.
 Fluid level. (by plain, C.T., T2 MRI)
 Osteomeatal complex.
Complication of acute sinusitis
1-Empyema, mucocele.
2- Osteomyelitis.
3- Orbital cellulitis.
4- Brain abscess.
Chronic sinusitis:
Thickened mucosa.
 bone density.
 Obliteration of sinus cavity.
(Mucocele expansion with no destruction + loss of translucency of the sinus)

Benign tumors:
- Ivory osteoma.
- Inverted papilloma : from middle meatus of nose  antrum
(histological name)
- Fibrous dysplasia: ground glass radiolucent area with island of
calcified bone.
- Ossifying fibroma.
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Malignant – tumors ( carcinoma & lymphoma ):

-Usu. From Med. Wall of antrum – Adeno or sq. cell c.
-Plain X-ray changes:
(1) Complete loss of sinus translucency's.
(2) Bone destruction. (diagnostic).
(3) Soft tissue mass in nasal cavity.
(4) Bowing of the nasal septum.
-CT value:
a.Extension: - Cribriform plate  Ant. cranial fossa.
- Orbit.
- Pterygopalatine fossa  Middle cranial fossa
b.Resp. after radiotherapy.

D.D of opaque maxillary antrum :

1- Traumatic: fracture( blow out).
 post operative washout.
 soft tissue swelling.
2- Inflammatory: - infection.
- infected mucocele.
- allergic  polypoid mucosal thickening.
3- Neoplast : - carcinom.
- lymphoma.
- Juvenile angiofibroma .
4- Miscellaneous: -fibrous dysplasia.
-cyst.
-Wegner granulomatosis.

N.B. Ch. haemolytic anaemia (imp.) Dr.Hoda (Mal developed sinuses + rodent face).
Proptosis in child  Hand – Chuller – metast. from Neuroblastoma.