Urology Handout

List of abbreviations Used

Predisposing factors
aetiology
due to
According to
Most Common
Characterized by

Between

Maybe -- with or without

Disease
Tumor
(Benign) / ( Malignant)

Movement
Fracture → Standard*

Antibiotics

Drug of Choice

→ Very Important Questions

*Standard →seen in textbooks & papers

-Any Emoji → ‫للمعرفة فقط‬

 Curriculum of Urology
Congenital anomalies→ Upper & Lower tracts *VIQ→
Trauma* →Renal trauma* -Ureter -Bladder - Urethra ‫موضوع مهم بييجي في النظري‬

Inflammatory → UTI
Neoplasms*→ Renal tumors* (RCC & Wilms Tm) & Bladder Cancer*
BPH* (not Tm) - Prostate Cancer & Testicular tumors*
Others
-Case taking
-Symptomatology* (Hematuria, Anuria & Retention)
-Endoscopy -Laparoscopy
-Uroradiology
-Renal transplantation
-Urinary Stones*
-Hydronephrosis
Congenital Congenital Anomalies

►Upper urinary tract anomalies

►Lower Urinary tract anomalies

 Congenital anomalies
Upper urinary tract anomalies
1- Developmental Anomalies
Of No Supernumerary kidney
Solitary kidney
Of Site Higher
Lower
Ectopic
Of Size Congenital Hydronephrosis
Of Shape Discoid
Horseshoe → Renal fusion anomaly + Malrotated Kidney

S-shaped
Lobulated
2- Cystic Disease of the Kidney

[Hereditary "Dse ,Syndrome " & Dysplaisa,Neoplaisa & Miscellanous ]

Hereditary ADPCKD
ARPCKD
Nephronopthisis
Glomerulocystic Kidney Disease
Syndromes Tuberous Sclerosis [TS]
Von Hippel Lindau [VHL]
Beckwith Wiedeman
Meckel Gruber
Zelleweger’s
Bardet Biedl
Jounes Syndrome
Dysplastic UPJO
PUV
MCDK = Multicystic Dysplastic Kidney
Neoplasia Cystic Wilms
Multilocular Cystic Nephroma
Congenital Mesoblastic Nephroma
Miscellaneous Simple Cyst
Calyceal Diverticulum
Chronic RF
Medullary Sponge Kidney
 Multicystic Dysplastic Kidney [MCDK] Infantile Polycystic Kidney Disease [PCKD]
Nonhereditary disease. hereditary dse [ARPCKD] AR ~autosomal recessive

Unilateral multiple, non-communicating cysts of Usually bilateral

various sizes (Multicystic) the appearance in Infancy is variable,
from normal to few isolated cysts rarely a kidney
packed with cysts
‫في البداية الكلية شغال كويس ولكن في النهاية بتدهور وتنتهي بفشل كلوي‬
No evidence of identifiable renal parenchyma Preserved
(Dysplastic Parenchyma) Renal shape
Echogenicity
Cortico -medullary differentiation

Treatment
Previously→ Nephrectomy Before renal failure
Now→ Classic ttt is Conservative & Follow Up Refer to Pediatric nephrology for Renal Support
As it will be atrophied by time After renal failure
Renal transplantation
But If the MCDK is not disappearing or is Nephrectomy is C/I except if renal transplantation
growing larger, Nephrectomy may be necessary is possible

MCDK → Detected Prenatally after 16 w' of Gestation

- In some patients, MCDK may be confused with UPJ obstruction.
In children with ANH, the reported incidence of MCDK is approximately 4-6%
-The presence of unilateral multiple, non-communicating cysts of various sizes and no evidence
of identifiable renal parenchyma is characteristic of an MCDK
3-Antenatal Hydronephrosis [ANH] → Detected Prenatally

Most common abnormalities detected on prenatal US

reported in approximately 1-5% of all pregnancies.
Definition
Dilatation Pelvic Calcyeal System in Fetal Kidney
Grading of Hydronephrosis [SFU*] *Society for Fetal Urology
Grade 0: → Normal
Grade 1: splitting of Central echoes
Grade 2: Pelviectasis, normal calyces
Grade 3: Pelviectasis , caliectasis normal parenchyma thickness
Grade 4: Pelviectasis, caliectasis with parenchymal thinning

A/E
[Transient & 6Ureter Causes & 2 Urethera]
Etiology Incidence
Transient hydronephrosis → Most Common Cause Of ANH 41-88%
UPJ obstruction → MC Cause Of Postnatal Hydronephrosis 10-30%
VUR 10-20%
UVJ obstruction/megaureters 5-10%
Multicystic dysplastic kidney [MCDK] 4-6%
PUV/urethral atresia PUV→ MC Cause Of ANH in boys 1-2%
Ureterocele/ectopic ureter/duplex system 5-7%

Mnemonics
Any U for Ureter -10%
Obst. at Higher level to 30%
Middle level → " not Obst but Reflux " to 20%
Obst. at Lower level to 5% 10- 10 ‫اكيد مش‬
 Pelviureteric Junction Obstruction Vesicoureteric Reflux[VUR] Obstructive MegaUreter Renal Duplication /Ureterocele
[PUJO]
Def. MC cause of Neonatal Dynamic event in w' Urine is obstructive dilatation of Cystic dilatation of the
Hydronephrosis Retrograde flowing from Bladder ureter above an adynamic intravesical segment of
toward kidney ureteral segment at UVJ ureter
Equal sex -More common e' duplex
Side –– Uilat or Bilat Kidney
-When associated e' Single
System → Uretercele
Commonly Intravesical
Diag Antenatal US Clinical
Ultrasound [US] # Lab. studies
Assess APD* of pelvis Radiological
MRU ± Cystogram -Voiding cystography [VCUG]––Diagnostic " Sometimes VU reflux only occurs while urinating (voiding)"
Renogram ## [Using MAG3] -DMSA**scan (Tc99m DMSA) scintigraphy → used to assess Renal parenchyma &Renal Scarring
Assess Differential(Split) Func. -US
Assess Obstruction
ttt First Assess risk 1-Medical Temporary ttt Incision
To avoid Hazards of VUR until surgery w' is after 1y' Urinary Diversion MCQ
If APD >3Cm & Split func. <40% Antiseptics- [Cutaneous Ureterostomy]
Pyeloplasty Voiding instructions
If APD <3Cm & Split func. >40% Anticholinergics. Permenant ttt
Not at risk 2-Endoscopic –– temporary ttt Uretrovesical Reimplantat***
if medical not enough
Just Follow Up→ /3m' Do U/S Ureteral submucosal injection e.g: *Anteroposterior diameter
If APD is Static or Decreasing **Dimercaptosuccinic acid (DMSA)
silicon →Bulking Agent
Follow up ***Not Done before 1y'
3-Surgery [ Ureteral re-implant]*** [As No Bladder Surgery before 1y' Except Bladder Exstrophy] why??
If APD is Increasing
Indications: d2 immaturity p Bladder &Achieve maturity after 1y'
Pyeloplasy #Postnatal US → Done after 1w' not in day Zero Why??
-Breakthrough UTI
To avoid false -ve d2 probability of improper feeding & dehydration
-Noncompliance e' medical ttt in 1st week so Urine not formed enough to produce detectable dilatation
-Grade IV or V, with pyelonephritic
changes ##Renogram Not done before 1.5 m' (45day)
due to immaturity of Kidney & Liver
-Deterioration of renal func
-Reflux that persists in girls at
puberty
VUR
►Pathogenesis of Refllux (Aetiology)

Disturbed Antireflux Mechanism

1ry VUR 2ry VUR

Anatomical Cause Functional Cause
due to anatomical abnormality of due to abnormal bladder function &
vesicoureteric junction elevated intravesical press

-PUV [post. Uretheral Valve]

-Short submucosal tunnel*
‫السبب الوحيد في األطفال‬
[Most Common Cause]
- Neuropathic bladder
- Prostatic Enlargment ~ [BPH]
*Intramural length of the ureter "Intravesical Segment" is too short.

► Hazards Of Reflux (Complications)

Persistent UTI.
Voiding dysfunction.
Failure to thrive [FTT] ‫للمعرفة فقط‬

Renal scarring. ‫ُدرست في االطفال‬

Renal failure.
Lower Urinary Tract Anomalies
 Bladder Exstrophy(+ Epispadias) Posterior Urethral valve[PUV] Hypospadias Epispadias
Hypo-below, spadon-orifice
=Ectopia vesica Detected Prenatally
1:10,000 -- 1:50,000 live births 1:8,000 live births. 1:300 Male —MC ?! 1:30,000
Males ONLY Why?? 1-Associated anomalies:- Male >Female
Risk of recurrence in given family UDT -- 9%
about 1:100 (500-fold increased risk) The female homolog to Hernia -- 9%
male verumontanum from which the 2-Abnormal karyotypes:-
Epidmology

valves originate is the hymen

Pt. with severe degrees (5%)
MC cause of lower urinary tract Associated cryptorchidism (22%)
obstruction in male neonates 3-Syndromes (49%):-
Single MC urologic cause Of Micropenis & cryptorchidism
Renal failure & need for (80%)
Renal transplantation in children MCQ MC associated anomalies in Hypospadius → undescended
testis [UDT] So don't forget Scrotal examination
Imaging Classification [Types]
Epispadias is mild form of bldr 1-US** ––––– → 1. Distal 50% 1-Complete type
exstrophy 2-VCUG 2. Middle 30% Associated e' Bldr exstrophy
& in severe cases both condition coexist [Diagnostic] 3. Proximal 20% 2-Incomplete type
3-Renogram Associated e' Normal Bldr
Complete ventral defect of UGS* -Antenatal diagnosis (70%) Ventral opening of ext. meatus Ant. Displacement of
& overlying skeletal system → "Key-hole sign " Ventral curvature. Urethra
Ant. displacement of posterior wall  Bilat. hydronephrosis Ventrally deficient foreskin Dorsal meatus
of bladder & trigone (MC Cause of ANH in Boys) Voiding & Sexual dysfunction Dorsal curvature
Mucosal edges of bladder fuse  Distended bladder Short phallus
Clinical Feature

with skin
Wide separation of the pubis
Epispadias
There's no continence
*UGS= urogenital sinus
Associated anomalies
 ±Oligohydramnios~ Hypoplasia Incontinence
Neonate
Palpable abd. mass
(Distended Bladder & Kidney)
Ascites d2 Obstructive Uropathy
Pul. Hypoplasia "Resp Distress"
-Older children
UTI &Voiding dysfunc. [Incont.]
**Postnatal U/S done in day Zero only for this Pathology [PUV]
 Bladder surgery day 0-3 (The only
one*)
❖ Staged reconstruction
1st Stage →Bladder closure
if older than 72 h' (3d')**
pelvic osteotomy (cutting bone to
correct deformity) e' Ext. fixation
2nd →Repair of episapdias
3rd →Bladder neck reconstruction
❖ One stage reconstruction
Treatment
–Initial Management
"For Urine retention/high SCr"
-Urinary drainage by Catheter
-ABx
–1ry (Transuretheral) valve
ablation or Incision
–Temporary Urinary Diversion
"If the infant is too small for safe
instrumentation"
Age of repair (6m – 1 y) # Surgical
Time of 2nd intervention ## ttt
(at least 6m' interval)
Goals of management
There is < 300 different techniques but all aim for
1. Anatomical looking:
- Straight penis
- Conical glans
- Slit like meatus at the tip
2. Functional normal urethra with
ability to direct a forceful stream

Elements of repair
-Vesicostomy Orthoplasty (straightening)
• Selected cases are suitable for - High loop ureterostomy Meatoplasty and Glanuloplasty
one-stage repair but other cases
Urethroplasty
require 3-stage
Skin Cover
Scrotoplasty
One stage Vs Staged repair ##?
Don’t Forget!
1-Scrotal examination
2-No circumcision before repair
Why ??***
3-PreOper. Hormonal therapy
4-PostOp. Care
MC Complication--Ureth.Cut.Fistula ##
* No Bladder Surgery before 1y' Except Bladder Exstrophy
**Why 3d' [72h'] ?! d2 presence Maternal Elastin H. – produce some sort of elasticity –Easy for Approximation of Pubic Bone but after 3d' ,pelvic osteotomy needed
***because the skin of prepuce can be used for repair––––new urethra is fashioned using neighbouring skin from prepuce or penile skin.
# Age of 6m' Why?–––– Highest success rate &Go to OR [Operation Room] e'out harm to psychology & Cognition to baby [Proper mother child separation]
## Time of 2nd intervention ------ Staged repair(if 2stages ---2nd stage done 6m' later) Also Repair of Fistula after 6m'
Complications Of Circumcision [ Incidence 0.2 - 2%]
 Hge 50% , 25% require hemostatic suture

 Urinary retention

 Wound infection
Urosepsis and meningitis
Necrotizing fasciitis
Sloughing of the penis

 Wound dehiscence or
denudation of penile shaft.
Urethrocutaneous fistula

Glans injury

Inadvertent circumcision of neonate with hypospadias

Foreskin abnormalities

Phimosis Paraphimosis
Def. The contracted foreskin cannot be The foreskin once retracted over the glans
retracted over the glans due to chronic cannot be placed again in its normal position.
infection
ttt ABx ± slit incision and later Circumcision Conservative & Slit Incision ± Circumcision
Hypospadius ~MCQ
Traumatic Urological Injury
►Upper urinary tract trauma
Renal – Ureter
►Lower urinary tract trauma
Bladder – Urethera
 Upper Urinary Tract Trauma Lower Urinary Tract Trauma
Renal Ureter Bladder Urethera
MC injured organ of Urinary tract •Traumatic 25% Cause Incidence % 1. Post. urethral injuries
50% of genitourinary trauma. •Iatrogenic 75% •blunt injuries[MC] 60 - 85% Intrapevic→ Memb. & Prostatic
10% of Abdominal trauma •penet. injuries. 15 - 40% • 10% of pelvic Fx*
•Blunt trauma→ 90% of Renal injury
Incidence

•pelvic Fx* • 90% of urethral injuries

10 - 29%
PDFs [also + Urethral inj] associated e' pelvic Fx*
1-Renal pathology (hydronephrosis, Tms) 2. Ant. urethral injuries
2-More common in children •C/S 0.3% Extrapevic →bulbous &penile
[d2 Weak support & Relative larger size] • bladder biopsy 30%(High) • Less commonly diagnosed
Larger→Exposed {Outside Protection** of Ms emergently
& Ribs }
1. Blunt trauma [90% of Renal inj.] ~MC 1.Traumatic [25%] 1. Blunt trauma: Post. Inj. Ant. injury
•Direct blow(sports, assaults, Anim kick) • Blunt trauma 10% of pelvic Fx* •Pelvic Fx* • Blunt trauma
•Rapid deceleration • Penet. trauma 2. Penetrating trauma: -Falling astride
-Motor car accidents gunshots or stap wounds
•Iatrogenic -Perineal trauma
Aetiology (Types of Trauma)

-Falling from height 3. Iatrogenic:

• Obestetric*** (catherteriza
Usually of minor degree •Penet. trauma
tion)
–Conservative ttt is usually successful 2. Iatrogenic [75%] [MC Iatrogenic Cause]
2. Penetrating Trauma • Gynecologic Surg. • Gynaecological
• Urological *Fx =Fracture
•Stab wound (Hysterectomy)
[MC Cause previously] • Orthopaedic
•gunshot
•Urologic Surgery 4.Idiopathic in Extremes of age
Higher degree of Renal damage
(Ureteroscopy, →After trivial Trauma
Usually associated e' inj. of other organs
Ureterolithotomy) Extraperitoneal rupture bldr
-Renal exploration is usually necessary
[MC Cause Now] • Fx pelvis is usually the cause
3. Iatrogenic injury
•Open Surgery
•General Surgery Intrapertoneal rupture bldr
Nephrolithotomy
•Endoscopic (Sigmoidectomy) •Direct trauma when the
PCNL [Percutanous Nephrolithotomy] bladder is full is usually the
cause

**Kidney Protection →  Located deep inside the abdomen  Surrounded by perinephric fat, lower ribs and back muscles has a range of vertical mobility
*** Don't Start Obestetric or Gyn. Surgery before fixation of A Uretheral Catheter Also Ureteric Catherization To avoid them during Surg. [One Vertebrae]
 Hx of: 1. Intraoperative Presentation Pathophysiology
• Trauma • Urine leakage in operative field Extraperitoneal rupture bldr Posterior injury
to back/flank/lower thx /Upper abd. (clear fluid) • Fx pelvis is usually the cause •Shearing Mvt of memb.
• Falling from height 2. Early Postoperative
Motor car accident • Extravasation occur at urethra against fixed
a) Leakage from a divided ureter perivesical space & prostatic urethra
• Gun shot, stab
Leakage either: may extend up to Ant. Abd. wall ►Pelvic hematoma &
Symptoms • Intraperitoneal [If urogenital membrane is inj.] displacement of prostate
• Hematuria [in 90% of cases] Sterile urine Infected urine upward
Intraperitoneal rupture bldr
→Absent in Tachycardia, Peritonitis, •Direct trauma when the Anterior injury
-Superf. Injury Fever, ileus Septicemia
Clinical Picture

bladder is full is usually the

-Thrombosed Renal Ar. • Extraperitoneal Ranging
cause
-Ureter Obstruction by Clot -Mass in the pelvis or the loin • Associated e' electrolyte
from just contusion
-Avulsed Renal Pedicle (Urinoma) disturbance [So ] to complete inj[Laceration]
(So not proportionate e' severity) -Leakage from • may passed unnoticed ►Extravasation could
• Flank pain wound, vagina or the drain for a long time extend up to Ant. Abd.wall
• Shock
b) Ligation of the ureter Clinical Picture
Examination • Loin pain & Fever • Hx of trauma / Surgery • Hx of trauma
• Signs of Hgic shock. • Gross Hematuria
• Anuria [if 2 Ureters were ligated] • Hematuria
• Contusions* over the flanks.3. Late Postoperative • Inability to void • Inability to void(retentio)
• Fx of the last rib. • Urinary fistula. Catheter→Bl. ± Little Urine • Blood at meatus
• Diffuse abdominal tendernes • Hydronephrosis d2 Ureteric strict. Intra [No Urine No Desire] [Pathognomonic]
• Flank Mass (hematoma, • Renal function impairment ‫المربع ده للمعرفة فقط‬ ►Evidence of Extravastion
Urinoma, Renal Tm) • Suprapubic pain ►DRE→ Upward
• Abdominal tenderness displacement of prostate
Early: •Urinary extravasation 1. Hge 1. Incontinence
• Hgic shock (Intraperitoneal or extraperitoneal) 2. Impotance
Complication

•Perirenal Urinoma or hemato 2. Pelvic infection

Late: ↓infection 3. Peritonitis 3. Stricture Urethra
• Perinephric abscess • Infection [MC Late Complication]
• HTN (Ischemic part of renal • Fistula (Uretero-vaginal or 4. Some degree of Urge
parenchyma) cutaneous) incontinence
• Urinary fistula • Stricture
• Hydronephrosis (PUJO**)
*Contusion = Bruise ---but Bruise better to be used in Skin **PUJO→d2 Fibrosis around kidney (Stricture)
Summary Of Complication →  Escape Of Bl. Or Urine [Early]  Infection of Escaped & accumulated Bl. Or urine ---- Heal Problem (Fistula /Stricture) [Late]
 1.Clinical 1.Clinical 1. Clinical: 1. Clinical:
(Mention) (Mention)
2.Radiological* 2.Radiological 2. Radiological 2.Radiological
C.T. Scan (pre and post contrast): CT:
MCQ Study of choice in renal trauma Investigation of choice for of CT scan Retrograde
abdominal trauma. =Ascending
• Grading of the trauma
(more sensitive than IVU) • It can reveal  Ascending cystogram Urethrography
• Perirenal anatomical details[Collections] Hydroureteronephrosis
Heamatoma, urinoma Collections (blood, urine) ↓
•Detection of associated injuries Urinary fistula. Both are diagnostic tools
e.g. trauma of liver, spleen, and pleura
•Determine condition of contralat. kidney IVU:
• Hydroureteronephrosis
Diagnosis

IVU** no contrast excretion

• Very poor sensitivity for penetrating Inj. contrast extravasation.
Urethral Injury
• Limitations in grading of renal injuries: →Suspected By
-Can’t detect minor injury. { ‫{اقل حاجه‬ Retrograde uretropyelography 1-Classic Triad
-If there is avulsion of the renal artery, (=Ascending Pyelography) • Inability to void
no contrast excretion {grade ‫{اعلى‬ for diagnosis of: • Blood at meatus
-No information about • Level of injury.
•Palpable Full Bldr
other organs or Perirenal collections • extent of ureteral lesion
• ± Stenting of the ureter 2-Catheter
Selective renal artery angiography & Can't Pass easily
embolization
Urography/Pyelography [3Types]
Indicated in ‫بينزف على طول او عمل وصله مع وريد‬ Ar 1- IVU=IVP=Excretory Urography
Catheterization →C/I
-Persistent or recurrent hematuria. Fix Suprapubic catheter
2-Retrograde Urography
- AVF [ Arteriovenous fistula] 3-Antegrade Urography
e.g. after renal surgery or biopsy. Graphy →Imaging e' Contrast
-alternative to surgery in poor risk patient.
*Also Renal U/S ------ Used in Conservative ttt for Monitoring Size of Hematoma [Collection] every d'

** One-shot intraoperative IVP --- Indicated When Unexpected retroperitoneal Hematoma seen in abd. Exploration
→ provides information for decision making concerning the injured kidney as well as presence of a normal functioning kidney on the contralateral side
 a) General ttt 1.At time of operation 1.Extraperitoneal rupture 1. Posterior injury:
AntiShock measures (resuscitation) • Immediate repair •Conservative 1. ttt of shock
A , B , C [IV line] ,D [Splinting of Fx] [In Most of the cases]
+Urethral catheter and NGT 2.within 5 d'& stable pt. fixation of Urethral catheter 2. Immediate Repair
+Bl. samples To determine Hb & SCr etc. • Re-exploration for 7-10 d' Endoscopic or Surgical
b)Local ttt & repair of Ureter. 3.Divrsion & delayed repair
1. Conservative ttt • Surgical intervention →best results
Grades I-II-III & IV {if hemodynamically stable} 3. After 5 d' must be done if •Suprapubic diversion
• Bed rest, IV line, Bl. transfusion if or debilitated patient -Hemodynamicaly Unstabl either percutaneous or
necessary • Control Urine leakage -associated other Organ inj. via open cystostomy*
• Analgesics & ABx to prevent infection of with temporary PCN* or -Large Vesical Hematoma •Repair [4 - 6 w' later]
Hematoma Double-J stent. -Injury to bladder neck via perineal incision
• Monitoring of -Vital signs/6 h' [Clinical] • Then delayed ureteral )Avulsion of bldr neck)
-Size of Hematoma /d' By Renal US[Radio] reconstruction after 3 m' 2. Intraperitoneal rupture Results ‫الفاصل بينهما هو‬
- Urine collection to assess its color [Lab.] • Surgical repair [urgent]
2. Surgical ttt
treatment

4. ttt of Complications [1st choice in most of cases] 2. Anterior injury:

Grades IV {if unstable or d2 penetra. Trauma} &V 1. Blunt trauma
a) Reconstructive: •Contusion→ conservative
• Excision of nonviable tissue. •Partial or complete tear→
• Repair of the renal tear.
FollowUp
1. Urethral catheter Urinary diversion &
b) Nephrectomy: Assessment few weeks later
• Irrepairable multiple parenchymal inj. must be left 10 -14 d'
2. Ascending cystogram • ttt of extravasation if occur
• Major vascular injury. 2. Penetrating injury
done before removing
• Life saving in severe Hge. *PCN= Percutanous • Up to 2 cm of bulbos ureth
catheter
Indications of Surgical exploration Nephrostomy & 1.5 cm of penile urethra
3. Suprapubic tube left
1.Hemodynamic instability [d2 Renal
till patient void successfully -Immediate repair &
bleeding] debridement to excise all
4. The patient could return
2.associated injuries (Spleen) PCNL = Percutanous
to work 4 - 6 w' later devitalised tissue
3.Pulsating or expanding hematoma Nephrolithotomy
PCNL → Nephroscopy
4-Grades IV [If d2 Penetrating trauma] • If more tissue is lost
5. Grade V renal trauma. -Delayed repair is advised
6. [Avulsion of renal Ar. or V. by CT]
7. Incidental renal pathology requiring tissue loss ‫الفاصل بينهما‬
exploration.
Summary of ttt → Conservative (in w' Tear spontaneously heal) Vs Repair of Tear (Immediate Vs Delayed) *Cystostomy [not cystotomy]
Classification of Renal Injury (American Association for the Surgery of Trauma) ~ AAST
CT Grading of Renal Injury {CT e' Contrast}

Grade I Contusion*

Conservative ttt
Hematoma Nonexpanding subcapsular
Grade II Hematoma Nonexpanding perirenal
Laceration** Cortical < 1.0 cm with No urinary extravasation
Grade III Laceration Cortical > 1.0 cm with No urinary extravasation
Grade IV Laceration Through Cortico-medullary junction Reaching collecting system

Grade 4 if Unstable or d2 Penet. trauma

& urinary extravasation
Vascular Main renal Ar or V. injury with contained hematoma
Laceration or thrombosis of a Segmental Ar.

Surgical ttt
Grade V Laceration Multiple deep Lacerations Compelete Shattered Kidney
Vascular Main renal Ar thrombosis
Avulsion of the renal pedicle Renal hilum = Renal pedicle

Grade I: No Laceration (No Parenchymal Injury)

Major trauma: (Grade IV and V) ~ often require Surgical Exploration
*Contusion → type of hematoma in tissue itself in w' capillaries and sometimes venules damaged & Caused by trauma
** Laceration[Tear Superf. Or Deep] → Parenchymal Injury Con -‫ & جوة‬Tusion- Tissue ‫ مثل‬Con ‫جوة‬Genital –Genitalia ‫الرحم‬

90% Rule for renal trauma

•Blunt trauma is the cause in 90% of patients.
• Minor grades are present in 90% of patients.
• Hematuria is present in 90% of patients.
• Conservative ttt is successful in 90% of patients
Inflammatory Urinary Tract Infection

►Upper UTI
Renal [Pyelonephritis]
►Lower UTI
Bladder [Cystitis] - Prostate [Prostatitis]
►Perinephric Abscess
 UTI
Bacteriuria Pyuria
Presence of Bacteria in Urine (any number) Presence of ≥5 Pus cells /HPF#
Urine →Normally No Bacteria [Sterile] especially in Bladder ►± Bacteriuria
►May be Asymptomatic or Symptomatic If e' out Bacteriuria [Sterile]

Asymptomatic→ Shouldn't be treated except if occurred

-During pregnancy → High risk of acute Pyelonephritis Pus Cells e' -ve Repeated cultures
-In Immunocompromised patient→ High Risk of Septicemia
(Causes ordered A2 Frequency)
Clinically significant pathogen concentrate 1-Stone dse (Esp. StagHorn) →MC
Clinical status or methods of sampling Significant concentration 2-Indwelling Catheters or Stents
(microbes / ml) 3-Urinary TB
-MSU*; 4-Early Bldr Tm (CIS)
urine in bladder <4 h
or symptomatic patient >103 CFU**/ml 5-Early Institution of ABx
6-Organisms not discovered by
Usual methods such as Virus /Fungi
-MSU; urine in bladder >4 h >104-5
-Asymptomatic bacteriuria >105
Catheterized Patient

- Male patient, catheter specimen sample >103

- Female patient, catheter specimen sample >104
- Suprapubic puncture sample any growth
{Used mainly in Children} ‫ من االطفال‬MSU ‫لصعوبة تجميع‬ Pyuria
"any Organism" -presence of [WBCs or Pus cell] in
Significant Bacteriuria Denotes UTI urine
Nonsignificant Bacteriuria Denotes Contamination -generally indicative of infection
and/or
inflammatory response of Urothelium
Def. oF Clinically Significant Bacteriuria ?????!!!!!!! ‫كالم المحاضرة‬ to the bacterium,
presence of bacteria in urine in No. Sufficient to produce Clinical Manifestation ?!!!! stones, or
other indwelling foreign body
± Pyuria
If e' out Pyuria →Indicate Bacterial Colonization e'out infection***
Or active Infection

* MSU= Midstream Sample of Urine #HPF =High Power Field

Discard the few early drops of Urine then collect the remaining, Don't Use (Local Antiseptics, ABx, Soaps)
** CFU=Colony-Forming Unit

***Infection = Invasion of tissues by Organsim → either Clinical or Subclinical infection

Colonization → presence of a microorganism on/in host, with growth and multiplication of the organism,
but without tissue invasion or damage
Contamination → Presence of a microorganism on a body surface or an inanimate object " microbiology sample "
introduced from an external source
 Urinary tract infections
Incidence → Common in but More Common in if

Classification

Non Specific UTI [More Common] Specific UTI

Subclassified A2 Site Specific Pathogen
Cause Specific pathology need Specific ttt
- Urethritis, Penis, Scrotum
- Cystitis Such as
- Pyelonephritis, Pyonephrosis -TB
- Epididymitis & Epididymoorchitis - Bilharziasis
- Prostatitis

Uncomplicated [Simple] UTI Complicated UTI

‫ أربعة شروط‬UTI Associated e' either
▪ Occasional (First / Isolated infection) - Anatomical abnormalities of UT as Stricture, Stone, Enlarged Prostate
▪ lower UTIs in Women - Functional abnormalities as Neurogenic Bladder, VUR
▪ No predisposing factors
▪ Recurrent*
▪ lower UTIs [Cystitis, Urethritis] in
pregnant women
men
Children
▪ +Ve PDFs → (Stone, Catheter " Catheter induced UTIs")
▪ Upper UTIs [Pyelonephritis]
*Recurrent UTI  Def.→ > 2 attacks in 6m' or ≥3 within a year  Forms a) Bact. persistence b) Re-infection

A/E Recurrent infection ‫لو‬ ‫ حاجات التالية ← خاصة‬3 ‫الزم تبحث عن‬

Causative Organism (C/O) Route of Infection PDFs

Bacterial [MC] : Specific & NonSpecific Ascending [Most common] General
E-coli (80%) → Commonest From Vagina, Perineum, Perianal -DM [MC]
▪ 80% of primary care infections -Immunocompromised pt.
▪ 50% of hospital-acquired infections Blood -Chronic debilitating dse
Others: Septicemia in
▪ Enterococci immunocompromised pt.  Local
▪ Staphylococcus saprophyticus Lymphatic
Obstruction
▪ Klebsiellas Stones [MC in Adults]
▪ Pseudomonas & proteus (Rare & Serious*) Others
Indwelling catheters
VUR [MC in Children]
Parazitic: Bilharziasis
Protozoal: T.vaginalis
Helminthic: Oxyuris

*Very Serious → Once discovered, Must be treated for sufficient duration (5-10 d') with appropriate ABx
 Upper UTI Lower* UTI
Renal [Pyelonephritis] Bladder [Cystitis] Prostate [Prostatitis]
Acute Chronic More common in females Classification
Incidence

Esp. Honeymoon Cystitis Category

↑ in especially in
Childhood, Puberty I Acute bacterial prostatitis (ABP)
Soon after marriage, pregnancy Chronic bact. prostatitis (CBP)
menopausal II
C/O Route PDFs Mainly - VUR Predisposing factors
III Chronic pelvic pain syndrome**
Same as before but Same Same -Stone dse ▪ Incomplete emptying of (CPPS)
Aetiology

-Bacterial [E.coli]
-Previous Surgery bldr: → BPH, stricture III A: inflammatory
-Parasitic ▪ FB: → stone, tumor III B: non inflammatory
Bilharziasis only ▪ Colonization of perineal skin
↓ IV Asymptomatic inflammatory
by E.coli
T.vaginalis or Oxyuris ▪ Estrogen deficiency
prostatitis (AIP)
Not Cause Upper UTIs Postmenopause (histological prostatitis)
• FAHM • FAHM Main Risk Factor → DM
High Grade Fever + Chills & Rigors Low Grade Fever > 90% of Acute Prostatitis associated e' DM
± Nausea , Vomiting "Recurrent attacks"
•Loin Pain •Pain (dull aching) Acute Chronic
•Irritative Voiding Symptoms •LUTs [Cystitis Symptoms] •Pain in Suprapubic Region • High grade Fever + Rigors • Low grade Fever
[LUTS ~ 2ry Cystitis]
• Irritative LUTS •Perineal Pain (intermittent)
•Tender Loin on Examination
Clinical Picture

+ Frequency [Earliest Symptom]

Dysuria •Obstructive Voiding Symptoms
HTN & Anemia Urgency &Urge Incontinence
•Rectal Tensmus
Pathology  Strangury [Common] •Perigenital Pain
(Painful Frequent urination of DRE → &Prostatic Pain
interstitial inflammation
small Vol ) -Severe Tender prostate • Difficulty in
• Suprapubic tenderness -boggy swelling -Urination
Scarring Renal parenchym
(Tubules Then glomeruli) (if abscess is present) -Defecation
+ -Ejaculation
• Pyuria DRE →
-Tender prostate
• Hematuria [Not Common]

* Some authors also consider infections of the urethra (urethritis) and prostate (prostatitis) to be lower UTIs.

** Chronic nonbacterial prostatitis = Chronic pelvic pain syndrome

 Acute Chronic Acute Chronic
1-Clinical 1-Clinical 1-Clinical 1-Clinical D By Exclusion
e
2-Investigation
2-Investigation C
2-Investigation 2-Investigation - Urine analysis /culture Urethroscopy
h
Diagnosis

- Urine analysis /culture Culture of Organism → diagnostic inflammed posterior

- Urine analysis /culture → Pyuria - Urine analysis /culture
- U/S → detect if there is obstruction, Stone → Pyuria
for Bacterial Prostatitis
urethra r
- CBC →Leukocytosis
- CBC →Leukocytosis - U/S → Detect obst., Stone No CBC & No U/S
- U/S o
-VCUG in children ►Investigate for DM
Prostatic massage n
Used as Follow-Up in ICU If persistent symptoms pus cells & bacteria in
If leucocytic Count [to detect VUR] If no Hx of DM i
investigate for PDFs the prostatic fluid.
-Increasing → Bad Sign - CBC →Anemia > 90% of Acute c
Prostatitis associated e'
-Decreasing →Good Sign "Improving"
DM
General Supportive ttt of PDFs (stones) Same as Acute PN Same as Acute PN Reassurance***
Bed rest No Effect on
Antipyretics - Analgesic Chronic suppressive But ABx for 1wk But ABx for 4-6Wks Erection or Fertility
↑ Fluid Intake therapy -Fluoroquinolones +
[D.O.C*] Drainage of abscess if
Empirical ABx for 10-14 d' [2Wks] ‫عبارة عن‬ -Nitrofurantoin present -ABx for 8-12Wks
Long term Use of -TMP-SMX** {3m'}
-3rdGeneration Cephalosporin prophylactic ABx -α-Blockers
(IV/IM) To prevent recurrent UTIs -Anti-inflammatory
-Fluoroquinolones (Oral) to Prevent Further
Treatment

damage
Or Sulphatrimethoprim (Oral)

If patient Can tolerate Oral feeding → Oral ABx Nephrectomy

If pt. Can't tolerate Oral Feeding → IV ABx If Cause Refractory HTN
Pt. (Vomiting, Extreme of age, Hospitalized) Provided that the other
kidney is Normal
[On Shift from IV to Oral Must do Overlap]

For Children
-Cefatriaxone 80 mg/Kg/day

Empirical ABx→ Fluoroquinolones [D.O.C]

As it penetrates the prostate well
*D.O.C → Drug of Choice ** TMP-SMX = Trimethoprim/sulfamethoxazole *** Only Complication Recurrent UTI Every 3-6m'
► Rare Forms of Pyelonephritis → Emphysematous PN & Xanthogranulomatous PN
 Perinephric Abscess
Pus collected within Perirenal fascia

Formed of posterior renal fascia [Zuckerkandl fascia] & anterior renal fascia [Gerota fascia]

if ruptured →develop Paranephric abscess

A/E
Previously [Before 1945*] Nowadays
90% 15% 1ry Abscess (Blood Borne) now d2 DM or Immunocompromised
10% 85% 2ry Abscess (Direct Spread) From Kidney or Neighboring structures
-Renal abscess
-UT abnormalities like stone ,obstruction causing pyonephrosis
-Pleura
-Pelvic Organs
* Introduction of Penicillin

C/P as acute PN but exaggerated

Attacks of high grade Fever [Hectic Fever]

Severe Loin pain & tenderness

Investigation
► Urine analysis /Culture

► CBC → Leukocytosis

► KUB→ Oblitrated psoas shadow

► US & CT are diagnostic

CT → Localization of Abscess

determine abscess configuration (unilocular or multilocular)

Treatment as acute PN but

-ABx for 2Wks + Metronidazole (IV not Orally) →For anaerobes

- Oral not effective in Systemic infection

-Drainage of Abscess
Unilocular → PCTD [Percutaneous tube drainage]

Multilocular → open drainage

Neoplasm Urological Tumors

►Upper UT tumors
Renal tumors
►Lower UT tumors
Bladder tumors
►BPH (not Tm) - Prostate Cancer
►Testicular tumors
 Cyst Solid*
►Simple Cyst ►Fat
MC Renal Mass above age of 50ys
Present > 50% of population above 50ys - Angiomyolipoma [AML] →
Hamartoma Bg Tm can be diagnosed Radiologically
-Rounded & Regular 5% of AML have poor fat content
-Radiolucent -Lipoma
-Not Enhance (refuse to opacity after contrast)
-Rim or Claw Sign ►No Fat
-Adenoma (MC Bg Tm)
-Oncocytoma →
Bg Tm can't be differentiated radiologically from RCC
Mg Cyst
-Leiomyoma
It's formed after cystic degeneration of solid Tm
– Enhance -Hemangioma
-JG Cell Tumor→ Ch' by Hyperreninemic HTN**

*any solid mass in kidney &Testis considered Mg Until proved otherwise - Almost always a Solid renal mass in children is Mg
Also No Biopsy in kidney or testis except Suspected lymphoma
**Surgical HTN (Curable)→ + ↓↓↓ renin or Normal Renin
Conn's Syndrome [1ry Hyperaldosteronism] ---- Cortex (ZG)
Pituitary Cushing [Cushing dse] ~ACTH Dependant or Adrenal Cushing [Cushing syndrome] ---- Cortex (ZF)
Pheochromocytoma (Paroxysmal HTN)-----Medulla
+ ↑↑↑ Renin [Hyperreninemic HTN] RAAS (↑Renin→↑Aldosterone)
[2ry Hyperaldosteronism] d2 Renal Ar. Stenosis or Renal Mass (Cyst or Solid) Compress BVs

Suprarenal Medulla → Bg Tm (Pheochromocytoma)

Mg Tm (Neuroblastoma)
 Benign Neoplasms Malignant Neoplasms
Epithelial
-Adenoma (MC Bg tumor)
-Papilloma
Connective tissue
-Hemangioma
-Fibroma.
-Lipoma
-Angiofibrolipoma
-renal cell oncocytoma
Renal Cell Carcinoma [RCC]
=Hypernephroma= Grawitz Tm
2% of all cancers
MC Urologic Tm ~ MC Renal Tm
Most Lethal Urologic Tm*
►Age
Epidemiology
1ry tumors 1ry tumors
►Arising from renal parenchyma ►Urothelial Carcinoma (90%) "MC type abroad"
-RCC = Hypernephroma = Grawitz Tm (75%) [MC Mg Tm] [Previously TCC]
-Wilms' tumor (10%) ►Non-Urothelial Carcinoma [Non TCC]
-Leiomyosarcoma, hemangiosarcoma & lymphoma (5%) -Sq.CC→ 5%
►Arising from renal pelvis (Urothelial) -Adenocarcinoma→ 1%
-TCC Others→ Lymphoma, Rhabdomyosarcoma
-SCC & Pheochromocytoma ?!!!
-Adenocarcinoma (Very Rare)
2ry tumors 2ry tumors
Carcinoma of lung, breast & stomach Carcinoma of lung, Prostate, Colon & Melanoma
Wilms' Tm
Bladder Cancer
=Nephroblastoma
Incidence: 1/10,000 child Incidence 10:100,000
7% of all childhood cancers MC cancer in Men in Egypt#
MC pediatric Renal tumor ►Age
►Age (Median Age of Onset 3.5ys) Bilh. → 3rd -5th decades [20s-40s] Why Younger??

Usually presents after 40 years of age 1-10ys 10-20ys >20ys Nonbilh. → 5th -6th decades.
►Sex Wilms >RCC Wilms=RCC Wilms<RCC ►Sex Bilharz. Pathogenesis
♂ ♀ = 2:1 90% of cases < 6y ♂ ♀ = 3:1. 1-abnormal Mucosa
►Sex ♂ ♀ ►Race 2-High Conc. Of
•Sporadic [MC Form] white race > blacks. carcinogens
•Familial (1-2%)
►Occupation
1 • Bilateral in 5%
In Egypt: Farmers.
[Synchronous or Metachronous**]
Abroad: Aniline workers
Stage 5 ‫ و‬5% ← Bilat. ‫التنسي‬
Synthetic Dyes
*So Radical Nephrectomy remains the standard treatment for RCC * is MC cause of Cancer death [Most lethal] in Both ♂ ♀
** Metachronous = Consecutive *Most Lethal Urologic Tm
#Breast Cancer → MC Cancer in Women Worldwide & in Egypt RCC 30% Bladder 21% Prostate 12%
Prostate Cancer → MC Cancer in Men Worldwide Bladder Cancer → MC Cancer in Men in Egypt Prostate → MC Cause of death from genitourinary Tm in ♂
Testicular Cancer → MC Cancer in middle age [ () age 15 & 35 ] ~ Always misdiagnosed because it's not age of cancer d2 high incidence although low lethality
 ►Sporadic [ >95% of cases] The two-event hypothesis=two-hit hypothesis
PDFs (Knudson and strong, 1972) ►Risk Factors
•Unknown. Gene Mutation in both alleles of one of following genes
• Bilharziasis.
•Cigarette smoking -WT1 suppressor gene at 11p13
• Chronic UTIs
[Most Important Risk Factor] -WT2 suppressor gene at 11p15
If also the damage affects Surrounding genes, • Smoking [Most Important Risk Factor]
•Obesity
associated e' anomalies (Part of Syndrome) ↑ Risk 4 folds
•HTN
As carcinogens Excreted & Stored in
•CKD patients undergoing hemodialysis bladder
develop acquired cystic kidney disease, with
increasing risk proportionate to the number of → • Chemical carcinogens:
years on dialysis. 1. WAGR syndrome WT1 [11p13] Tryptophan metabolism
-Wilms' tumor (50%) Aromatic amines [Aniline dye]
►Familial Syndromes [2-3% of RCC] -Aniridia Fertilizers [Nitrosamine]
AD, Usually Bilateral, Multifocal, Early age of Onset -Genitourinary anomalies Drugs
•Von Hippel-Lindau [VHL] - Hypospadias Association ‫بينهم‬ [phenacetin1, cyclophosphamide2]
Aetiology

-bilateral renal cysts and cancers, - Cryptorchidism See Congenital anomalies •Chronic bladder stone & Obstruction
-pheochromocytoma, - Duplication of collecting system
-Mental Retardation & Indwelling Catheter
-Brain & retinal hemangioblastomas
•ADPCKD1 2. Bechwith-Wiedemann syndrome [BWS] WT2
(No increased risk of RCC) ‫ كل حاجه كبيرة ماعدا راسه‬Wideman ‫الراجل الواسع‬ Pathogenesis of risk factors
- Microcephaly see later
•Birt Hogg Dube [BHD] syndrome
25% develop RCC - Macroglossia, Macrosomia
- Visceromegaly ►Precancerous lesion
•Tuberous sclerosis [TS]
↓lead to -Dysplasia (Atypia)→ TCC, CIS
2% develop RCC
- Omphalocele [Exomphalos]-- Umbilical Hernia -Sq. metaplasia / Leukoplakia** →SCC
•Hereditary papillary RCC - Hemi-hypertrophy ‫نص جسمه ايد ورجل اكبر من االخر‬
•Hereditary leiomyomatosis RCC -Glandular metaplasia(Cystitis glandularis)
- Wilms' tumor (5%)
→ Adenocarcinoma
3. Denys Drash syndrome WT1 [11p13]
►Precancerous lesion Clinical ‫صعب تشخيصه‬ -Nephrogenic adenoma → Adenocarcinom
Renal adenomas may predispose to RCC - Wilms' tumor (90%) →usually bilat.
- Nephropathy→ Congenital mesangial sclerosis
1 Analgesic Removed from Market but still used as
- DSD [Disorder of Sex differentiation]
4. Isolated aniridia (30%). Herbal ttt
1
ADPCKD ~ Adult PCKD 2 its Metabolic product (Acrolein) cause Hgic Cystitis
[autosomal-dominant polycystic kidney disease] 5. Isolated hemihypertrophy (4-8%)
6. Isolated GU anomalies →↑risk of bladder cancer
Cystic dse of kidney **Advanced form of Sq. metaplasia with marked
Congenital (No risk) or Acquired (by dialysis) keratinization leuko~White plakia ~ plaques
*Survillence → over extended period of time Survey → at single point of time
Pathogenesis of Risk factors of Cancer bladder
1. Ch. Irritation theory (Furgson, 1911):
-Passage of bilh. Ovae → ch. Irritation of mucosa→ squamous metaplasia → bladder cancer.

-Carcinogen: A substance which is capable of producing irreversible changes in the mature cells.

2. Meracidial toxin theory (Makar, 1942):

-After death of ovae → Meracidial toxins which are carcinogenic.

3. Alkaline septic theory (Delbey & Moore, 1942): Urine Normally Acidic but alkaline urine irritative to bladder

-2ry infection with urea splitting organism Alkaline urine (Carcinogen) Proteus →Urease +ve
Split Urea into NH3 (Ammonia) → Strongly Alk.
4. Chemical theory:
a- Tryptophan

Normally Metabolized in liver: orthoaminophenols (carcinogen) Conjugated with glucuronic acid →

conjugated form excreted in urine [Non carcinogenic]

► In Bilh.:

-Liver cirrhosis: ↓↓ conjugation.

-Beta-glucuronidase enzyme (produced by bilharzial bladder) → Split the conjugated form liberating orthoaminophenols.

b- Aromatic amines: "Aniline"

Active sub: ,  naphthylamine (carcinogen).

Metabolized in liver: 2 amino-l-Naphthol (carcinogen) → conjugated with glucuronic acid →

conjugated form excreted in urine [Non carcinogenic]

-In liver cirrhosis: ↓↓ conjugation

(d2 HBV or HCV)

-↑ Beta-glucuronidase enzyme production.

c- Smoking

4-folds higher incidence than nonsmokers.

Carcinogens: tryptophan metabolism, Aromatic amines. Nitrosamine (Fertilizers).

5. Badr (1964)
Combination of 1, 2,3, 4.

a. Local factors → Anaemic bladder wall, mucosal changes.

b. Systemic factors → Carcinogens

 From PCT ??? ‫ ورق‬MCQ Embryogenic cells (Primitive Metanephric *Orgin of adenocarcinoma [from Col. Epith.]
tissue) → totipotent cells 1-Cystitis glandularis
From Renal tubules "‫من الباوربوينت "كالم علمي‬ 2-Nephrogenic adenoma "Precancerous Lesion"
Origin

PCT→ Clear cell & papillary RCC

DCT→ chromophobe & Oncocytoma* RCC
*Oncocytoma is Bg Tm cannot be differentiated
radiologically from RCC.
-Bilateral (2-3%) more e' familial forms
Site
-Congenital → Ectopic kidney tissue*
-Acquired→ Chronic infection
3-Patent Urachus1(Urachal Carcinoma)
4- Urinary Diversion [as Ureterosigmoidostomy]
*
Failed to ascend & embedded in wall of bldr
-Arise in one pole → usually Upper pole 1- Post wall: 35% MC Site
-Bilateral (5%) 2- Lateral wall: 30%
Stage 5‫ و‬5% ← Bilat. ‫ التنسي‬3- Anterior wall: 25%

4- Vault: 5%
5- Trigone 5% → Worst prognosis
Mg Anuria & Bilat. hydronephrosis
NE (Morphology/Gross appearance) NE (Morphology/Gross appearance) NE (Gross appearance)
Solid mass pseudo capsulated e' areas of Hge &necrosis Bilharz. Non bilharz.
A solid mass which is well-encapsulated (Pseudo ME (Histology) •Nodular fungating MC Type •Papillary MC
capsule) Triphasic Tm •Papillary "Cauliflower" •Nodular
-Cut Section -Blastema → undifferentiated small* blue** Cells
-Ulcerative -Ulcerative
• golden-yellow color -Epithelium → tubules
Fibrillary2
• Variegated appearance (Multiple Color) -Stroma
• radiating septa → lobulated ►Histological types ME (Histology)
• areas of Hge, necrosis or cystic degeneration. 1. Favorable histology [95%] Bilharz. Non bilharz.
Pathology

It may penetrate the renal capsule. • Non-anaplastic Wilms' tumor S.C.C 50-60% T.C.C 80-90%
±Tumor extend or prolapse into renal vein or IVC 2. Unfavorable histology [5%] T.C.C 40-50% S.C.C 5-10%
Why?? because Renal Tm under High Press.
• Anaplastic Wilms' tumor Adenocarcinoma* 2%
d2 20% C.O.P -Hypervascularity - Squeezing by Diaph
-Aggressive, rapidly metastasize Incidence of
ME (Histology)
→Adenocarcinoma
- Chemo resistant TCC ~ ↑↑
• Clear cell subtype (75-90%) MC type • Clear cell sarcoma of the kidney (CCSK) d2 pollutions & Smoking
Best prognosis • Rhabdoid tumor of the kidney (RTK) SCC ~ ↓↓
• Papillary 10-15%. Worst prognosis "High morbidity" Bilharziasis ↓↓
• Chromophobe 5% *small d2 rapidly multiplying **blue d2 little or no cytoplasm
d2 -easy & available ttt (just 4 tablets)
• Spindle shaped Cell -Chemicals from manufactories kill Snails
Worst prognosis
1 Urachus → Developed from allantois →Convey Urine from fetal Bladder Through Umbilicus into Yolk Sac → Normally obliterated after birth as Median umbilical Lig.
2 Fibrillary type →as tuft of hair [low stage, low grade, low incidence of Mets --- Best prognosis]
Grading Fuhrman nuclear grading (I -IV) WHO Grading (I-III)
Nuclear based (A2 Size of Nucleus) Grade I [Well differentiated]
II [Moderately differentiated]
III [Poorly differentiated]
1- Direct → adjacent organs 1- IVC 1- Direct
2- Lymphatic → Lymph nodes 2- Lymphatic
Spread

2- Lymphatic → hilar and para-aortic LN "as testis" •Regional LN "below bifurcation of common iliac"
3- Distant metastases → [ Obturator - Hypogastric - Ext. iliac -Presacral LN]
3- Distant metastases → Lung [MC] - Bone – Brain Lung – Liver •Nonregional/juxta regional LN "above bifurcation"
Bone – Brain (only in CCSK &RTK) 3- Blood Common iliac LN
T (1ry Tumor) Postsurgical Staging T (1ry Tumor)
T1 Tm 7 cm in greatest dimension, limited to ‫ ا‬Tx Doubtful diagnosis
kidney T1a <4 cm T1b 4-7 cm a) Stage I (40%) →Organ confined Ta Mucosal lesion (papillary)
T2 Tm 7 cm in greatest dimension, limited to Tis Carc. in situ [CIS]~Flat lesion
►Clinically no
kidney T2a 7-10 cm T2b >10 cm b) Stage II (22.5%) →Beyond the T1 Invasion of lamina propria palpable mass
kidney but completely excised
T2 T2a: Invasion of superficial half of muscle layer.
c) Stage III (22.5%) → T2b: Invasion of deep half of muscle layer.
T3 Tm extends into perinephric fat or major veins Abdominal1 non-hematogenous2 ► Clinically Mobile palpable mass e' smooth surface
T3a Perinephric or sinus fat or renal vein
residual T3 T3a: Microscopic invasion of perivesical fat
T3b IVC below the diaphragm T3b: Macroscopic invasion of perivesical fat
TNM Staging

T3c IVC above the diaphragm •+ve LN ► Clinically Mobile palpable mass e' irregular surface
T4 Tumor grossly extends beyond Gerota’s fascia, •Tm Spillage →by Tm rupture/biopsy
including ipsilateral adrenal
•infiltrated safety margin T4 T4a: Invasive of adjacent organs. ► Hard fixed
T4b: Invasion of the pelvic wall mass
•Tm thrombus in renal v. or IVC
N (Regional LN = Nodal Metastasis) N* (Regional LN = Nodal Mets)
Nx: Doubtful diagnosis d) Stage IV (10%) →Distant Mets Nx: Doubtful diagnosis.
N0: No evidence of LN involvement e) Stage V (5%) → Bilateral N0: No evidence of LN involvement
N1: Metastasis in Regional LN Stage 5‫ و‬5% ← Bilat. ‫ اكيد نسيت‬N1: Single Regional LN in true pelvis Mention
N2: Multiple Regional LN in true pelvis Regional LNs
N3: LN Mets to Juxta-Regional LN [Common iliac LN]
►Nodal Mets above bifurcation~common
M (Distant Metastasis) M (Distant Metastasis)
iliac [N3] Considered Distant Mets [M1]
M Why? M
N1,2 → 5ys Survival = 50%
M M
while N3 → 5ys Survival = 10-20%
M ►Nl-3 equal to D1 in Marshal M Juxta-Regional LN
Grading→ for differentiation & Staging→ for Spread *laterality does not affect N classification (Unlike breast cancer)
Below Diaph→ Thrombus Can removed by
open IVC using Same abdominal Incision
Above Diaph →Need thoracoabd. Incision
& CardioPul. Bypass
 Symptoms 1. Abdominal mass (> 90%) MC Symptoms
1ry Tm Mets Paraneoplastic syndrome Malignant cystitis
Ch' by
•Rapidly growing huge mass causing abd. distension
Asymptomatic [50%] -Exaggerated Cystitis [Severe LUTs]
‫زي البطيخة‬
Incidentally discovered during imaging for non-related medical but painless d2 its gradual growth -No response to Simple line of ttt2
issues •Rarely Detected in small size except in
(ABx & Analgesic)
 Symptomatic [50%] -Surveillance of Syndromes
•hematuria (50%) → Early  •Irritative bladder symptom [LUTs]
-follow up of Contralateral kidney in unilat. wilms Tm
[Profuse, Painless, Periodic, Pan hematuria]
d2 early infiltration of renal pelvis 2. Abdominal pain •Hematuria1 (Common e' TCC)
•Loin pain (40%) d2 Sudden stretch of capsule by Hge inside Tm →Earliest Symptom
[Painless Intermittent hematuria]
•palpable abdominal mass (30%) → Late1 or Infiltration of nerves (advanced stage)
The classic triad of flank pain, hematuria & mass 3. Hematuria (25%) → Late •Necroturia (Common e' SCC)
is found in 10% of cases (advanced disease) → too late d2 late infiltration of renal pelvis Passage of necrotic tissues in Urine
►Paraneoplastic syndromes (20-30%)
Syndrome Cause Symptoms of Metastasis
HTN (40%) → MC Renin 4. HTN (25%)
Hypercalcemia (10-20%) PTH-like substance
C/P

Polycythemia (3-10%) EPO 5. Vascular extension (4%) [IVC Tm thrombus]

Stauffer syndrome (3-20%) GM-CSF* (Ascites, CHF, hepatomegaly, varicocele)
(reversible non-metastatic hepatic dysfunc) 6. Associated anomalies
-abnormal liver function tests
Syndromes & aniridia & hemi-hypertrophy, etc.
- high ESR
-high alkaline phosphatase
Pyrexia, cachexia, wt loss and neuropathy Examination
Cushing ACTH 2
if no response to Simple line of ttt within 7d' → Check DRE
Pituitary like

Decreased libido, balding, Gynecomastia ♂ Gonadotropins for the cause

hirsutism, amenorrhea ♀ [HCG] The greatest mistake is to treat hematuria with ABx -Many Stories of many cases
Galactorrhea Prolactin & assume that if bleeding stops,
Hypoglycemia Insulin yet not suspected to have
Infection was the cause without undertaking further
* Granulocyte-macrophage colony-stimulating factor bladder cancer esp. those
investigations.
PNS are reversible after tumor resection resistant to ttt
but their persistence indicates metastases and poor prognosis Detected by DRE even by PV
► Symptoms due to IVC Tm thrombus
•Non-reducing varicocele usually on Rt side with recent onset Remember
•Bilateral LL edema
1
bladder Tm → almost always detected early (T1 or below) Staging of bladder cancer
►Symptoms from metastases d2 early hematuria [Red Sign]
Clinically
lungs (75%), liver & Bones
1
unlike in hollow Organs, most solid mass in parenchymatous Organs [Liver, Renal, Prostate] → Detected late when Enlarge(Compress) or Infiltrate
 Signs (Physical examination) Renal testicular relationship →
During intrauterine life → testis descend while kidney Ascend
1ry Tm Mets Paraneoplastic syndrome
Usually unremarkable in incidental cases.

•Renal mass
testicular Ar Renal Ar
-In Loin (Most important Character)
Both from Aorta
-Irregular Both from Aorta
[Longer] Rt > Lt
-Firm or hard
-usually not tender

-Mvt with respiration & ballotment
are initially retained to be lost later (Fixed) Lt renal vein Longer & Higher Level than Rt
testicular V. Renal V.
•Dilated superficial abdominal veins Rt Drain into IVC Both drain into IVC
•Rt non-reducing varicocele [2ry Type] IVC Tm thrombus
Lt Drain into Lt renal v. Rt < Lt
Shorter Longer*
•Bilateral LL edema
Drain Rt kidney only Drain Lt Kidney, Lt SRG, Lt testis

•Lt supraclavicular lymphadenopathy →Mets Multiple Organs ‫ ل‬drain ‫ و‬Longer ← Lt renal v. ‫ ولذلك‬Lt Organs ‫ بعيده عن‬IVC ‫ شمال وبالتالي‬Ao ‫*عشان‬
Rt phrenic v. drain into IVC while Lt phrenic v. drain into Lt Suprarenal v. ‫وأيضا‬
Cardiothx ‫موجودة في منهج‬

•HTN

•Paraneoplastic syndromes
Common Innervation
So Renal pain refer to testis

drainage to same LN (To Paraaortic LN)
all Genitourinary Tm can be presented with Enlarged Lt supraclavicular LN
Unlike Rt supraclavicular LN which not affected except in Breast & Thyroid Tm

RCC →Most lethal Urologic Tm d2 occurrence in old age & Surgery is only line of ttt
Testicular cancer →Most Curable Urologic Tm d2 occurrence in young age & multiple lines of ttt
1- Spread (Mention) 1- Spread (Mention)
Complications

2- Venous obstruction →Varicocele or bilateral LL edema. 2- Ureteral obstruction → Uremia.

3- Paraneoplastic syndromes 3- Bleeding

 I) Laboratory Routine I) Laboratory
 Urine analysis→ Microscopic Hematuria  Abdominal US  Routine lab.
 CBC → (anemia1, polycythemia2) differentiate () solid & Cystic mass CBC, LFTs, SCr, Bl. sugar
 Creatinine, liver function tests, alkaline phosphatase, but can't differentiate () Bg &Mg Urine cytology → For Screening High risk
blood sugar, serum Ca If +ve [Mg Cells] →Perform Endoscopy &Biopsy
1
d2 Bl. Loss (hematuria) & 2 d2 Paraneoplastic [EPO release]  CT chest, abdomen & pelvis DNA flow cytometry*
II) Radiological or MRI For Prognosis & follow-up not for Diagnosis
 US → Initial Imaging For Staging & detection of Mets Reveal Curve of DNA distribution
Biopsy If Diploid/tetraploid→ Good Prognosis
differentiation () solid* mass & cyst of the kidney Only indication [Advanced Tm w not If Triploid/Pentaploid/Hexaploid→ Aneuploid**
 CT scan e' Contrast→ gold standard for renal mass candidate for Surgery] (Very bad prognosis)
-Assessment of 1ry Tm [Staging of renal Tm] *Cytometry =DNA ploidy
**Aneuploid =presence of an abnormal No. of chromosomes
-Assessment of function and morphology of contralat. Additional imaging in select
II) Radiological
kidney. Tm
-Assessment LN & Vascular Tree (Tm thrombus in IVC /Renal V.) • Only in CCS & RTK → KUB (UTP)
to detect associated stones or calcification
Investigations

-Assessment of Chest [accurate staging of Lung Mets], brain CT or MRI & bone scan
SRG & Liver of bladder
DDx of renal mass in children Abdominal US
AML →Bg Tm can be diagnosed by CT Scan d2 its fat content In full bladder→ Can detect masses
Oncocytoma →Bg Tm can't be differentiated radiologically from RCC
•Solid mass→ considered Mg [99%] Limitation of U/S is bone & gas so full Bladder
•Congenital Hydronephrosis act as window for pelvic visualization
→
•Cystic →  IVP [Intravenous pyelogram]
Single (Simple Cyst) -Evaluation Upper UT for associated urothelial Tm
 MRI Multiple
Used in allergy to IV Contrast or to assess Venous thrombus -On Cystogram phase → Can detect irregular filling
Unilat.(MCDK) defect - No Staging by IVP
 Chest X ray: lung metastases or pleural effusion Bilat. (PCKD) - Evaluation Ureteric Obstruction
 Bone scan, brain CT or MRI
 Bimanual EUA → for Clinical Staging
in symptomatic and advanced cases MCQ
Cystoscopy & Biopsy→ Diagnostic
 Biopsy Skeletal Survey Bone scan
Cystoscopy under local anesthesia.
unnecessary to avoid spread of Tm (Increase Stage) Plain X-ray Isotope
CT & MRI
-lymphoma is suspected Not sensitive Sensitive
except if -Evaluation Upper UT (more accurate than IVP)
-Advanced Stage w' not candidate for Surgery Specific Not Specific
-Proper Staging
+ve Bone scan
-Healing Fx & Old trauma T -Assessment of Nodal & Distant metastases
-Osteoarthritis I  Skeletal Survey ± Bone scan
-Malignancy N For detections of bone mets
-Paget
*Any Solid mass in Kidney Considered Mg
 [Most Important Prognostic factors → Staging & grading] ttt & prognosis depend on Stag ing & Histology
Poor predictors are • Stage I (FH*) → 95%
a- Clinical • Stage II & III (FH) → 90%
Localized symptoms, cachexia, anemia.
b- Pathological • Stage IV (FH) → 80%
High stage and grade, sarcomatoid features,
Prognosis

c- Biological
Abnormal DNA polidy. • Stage I-III (UFH) → 65%
vascular endothelial growth factor (VEGF) • Stage IV (UFH) → 50%
P53.
d- Therapeutic
Surgery remains the only curative line of ttt of RCC

The overall 5ys survival is 60% after radical nephrectomy, the *Favorable histology
presence of local spread or distant metastases is associated with
poor prognosis.

Gold Standard for

-PUV & VUR → VCUG

-Renal Trauma, Ureteric inj. → CT scan e' Contrast

-Renal Mass (including Tm) → CT scan e' Contrast

-Bladder & Renal Pelvis Tm [Hollow organs] →

Endoscope (Cystoscopy – Ureteroscopy) & Biopsy

-Prostate Cancer → TR -US & Biopsy

•
-Renal Stones → NCCT (spiral CT)

• CT scan → Left kidney shows an enhancing solid mass

 Surgical treatment is the only curative line of ttt of RCC All patients treated e' Non-Urothelial (SCC & Adenocarcinoma)
RCC[adenocarcinoma] So Chemo & Radiotherapy →Ineffective Combined surgery + Chemo ± Radiotherapy Chemo & Radio resistant→ so
A) ttt of Localized disease ►Radio only in Mets, Residual (IVC thrombus) the only line of ttt is Surgery
Radical Nephrectomy [Extra gerota nephrectomy] ►No & Duration of Chemotherapeutic agents [Radical cystectomy + Urinary Diversion]
●Includes Unlike Simple nephrectomy Depend on Tm Staging & Histology whatever Stage
-extrafascial removal of the tumor-bearing kidney ►Surgery for unilat Wilms' Tm If patient unfit for Surgery→ Palliative ttt
-Renal Ar is ligated before the vein Upper transverse abdominal incision. Urothelial Carcinoma
Enbloc removal of kidney & perinephric fat. Through exploration of the abdomen. Superficial Bladder Tumors (NMIC)
-SRG is removed when involved. • Radical nephrectomy & random LN sampling
►Ta and T1
-Sampling lymphadenectomy is helpful in staging. • Exploration of contralateral kidney
●Conservative ttt
Surgical approaches may be open, laparoscopic, or robotic. Treatment Protocols 1-TURBT ‫العالج بالمنظار‬
●the standard ttt for RCC with normal opposite kidney Surgery ‫وال‬chemo ‫ االختالف في الترتيب مين األول‬2-Intravesical Immunotherapy (BCG)
Radical Nephrectomy with Thrombectomy 1. SIOP (Europe) given in high risk cases
●Only line of ttt of Vascular extension (into Renal v.& IVC or even • 1ry chemotherapy {Chemo then Surgery} or Intravesical Chemotherapy (Mitomycin C)
Rt atrium) even if in Solitary kidney • No biopsy 3-Regular follow-up cystoscopy & cytology
Nephron-Sparing Surgery (NSS) 2. UK ●Radical Cystectomy indicated
●Includes Tm enucleation and partial nephrectomy • 1ry chemotherapy (failure of conservative ttt)
●Indicated [when need to preserve renal tissue] • Needle biopsy 1- Rapid Recurrence in time & place.

Progression
-Renal impairment [DM or HTN] 3. NWTSG (North America) 2- Tm changes from low to high grade.
treatment

-RCC* in a solitary kidney [*Provided that no vascular Extension] • 1ry surgery {Surgery then Chemo} 3- Tm changes from diploid to Aneuploid.
-Bilateral RCC e.g. Von Hippel-Lindau disease. Europe 4- Tm becomes invasive (invade Ms wall).
Advan. → DownStaging →↓ Intraoperative Complications
-Pathological or damaged opposite kidney. 5- Large, multicentric Tm beyond the scope
Disadvan.→ Unknown accurate Staging
-Incidental small RCC UK of resection.
Alternative investigational ttt Disadvan. → Needle biopsy ↑Stage from I to III ►Tis [Flat lesion]
●in patients unfit for surgery with small peripheral Tm North America---Done in Egypt becomes invasive in a large % of patients.
Advan. → Accurate Staging
►RFA [Radiofrequency ablation] ● Conservative ttt
High frequency electric current results in local heat. 1-intravesical BCG
►Cryoablation Preoperative therapy DownStaging 2-regular follow-up cystoscopy and cytology
destruction of tumor by rapid freezing Must Start with Chemotherapy  TURBT Not indicated
to do partial
►HIFU [High intensity focused US] - Bilateral tumors ●Cystectomy is indicated
nephrectomy -when Ms invasion is evident
US waves are focused into a small region causing heat - Tumor in a solitary kidney
B) ttt of Metastatic RCC - IVC thrombus above the hepatic veins -Recurrent multifocal CIS
Radical nephrectomy (whenever possible) - Inoperable tumor on surgical exploration Ms Invasive Bladder Tumors (MIC)
Surgery to an isolated metastasis Treatment of relaspe ►Organ Confined (T2 & T3)
performed when the disease is resectable & patient is fit. 1. Mostly in the 1st 2 years (11 years) ●Radical cystectomy + Urinary Diversion
Radiotherapy 2. Incidence: Standard of Care but 5ys Survival=50%
useful in symptomatic ttt of bone & brain metastases. - Stage I-IV (FH) 10-20% ●Chemo&Radiotherapy
Immunotherapy→ Poor results - Stage I-III (UFH) 30% Stage IV (UFH) 45% If patient unfit or unwilling for Surgery
Interferon-alpha 3. Site →Lung, Abdomen Results Unsatisfactory
lntcrleukin-2 (has more side effects) 4.Individualized ttt ►Non Organ Confined (T4 & Mets)
Targeted therapy and angiogenesis inhibitor drugs →palliative 5.Aggressive chemotherapy & BMT Palliative and /or Symptomatic
measures -Radio, chemo, Surgery or Combination
Some Notes on ttt of Bladder Cancers
-The greatest mistake is to treat hematuria with ABx & assume that if bleeding stops,
Infection was the cause e' out undertaking further investigations (Cystoscopy)
-Tumor is diagnosed by Tissue biopsy.
-Investigations are to evaluate the degree of extension of the tumor to select modality of ttt
Objectives of ttt
• Save life [Lethal Tm] → Survival
• Save function →Organ sparing
• Optimize QOL →Minimally invasive techniques

-TURBT (Trans Urethral Resection of bladder tumor )

Done by Rigid Cystoscope[therapeutic] not flexible [Diagnostic]
- Intravesical adjuvant therapy:
Types
 Intravesical immunotherapy (BCG)
Produce local aggressive immune reaction to invite inflam cells to attack any rapidly dividing cells [Mg Cells]
BCG should never be given in patient with Hematuria or known trauma to urinary tract such as immediately after TURBT
but given after 2Wks from TURBT d2 fear of systemic absorption[Systemic reaction] and sepsis
 Intravesical chemotherapy (Mitomycin C & Adriamycin)
Indications of intravesical adj. therapy in ttt of superficial Bladder Tm
1- High grade tumor.
2- Aneuploid DNA

3- Recurrent tumor
4- Multicentric tumor If Together treated by Radical Cystectomy
5-CIS
Regular follow up Cystoscopy & Cytology

/3m' in 1st Year

/6m' in 2nd Year
/year later

T2 & T3 → treated by radical Cystectomy not partial Even if small Tm as it become Unstable urothelium
Radical Cystectomy
Either -Open -Laparoscopic -Robotic

Indications

I-SCC & Adenocarcinoma whatever Stage

II-Urothelial Carcinoma
A- Superficial bladder Tm (NMIC) in failure of conservative ttt→ {Recurrence, Progression & Multicentric}

1- Rapid Recurrence in time & place.

2- Tm changes from low to high grade.
3- Tm changes from diploid to Aneuploid. Progression
4- Tm becomes invasive (invade Ms wall).
5- Large, multicentric Tm beyond the scope of resection

B- Ms Invasive bladder Tm (T2,T3)→ it's Standard of ttt

Includes

Pelvic LN dissection, with wide excision of bladder

Peritoneal covering, Perivesical fat 2 Covering

Pedicles, ligaments and lower ureters ‫وصالت‬

In Men → Vas, seminal vesicles & prostate.

In Women → Fallopian tubes, uterus, upper vagina & ovaries in postmenopausal
[in female Radical Cystectomy known as Anterior Pelvic Excentration]
Sparing One Ovary in Premenopause
Complications to maintain its Hormonal Function

 Mortality (1-3%)
 Morbidity(20-30%)

Bleeding
Pelvic abscess, sepsis
Small bowel obstruction
Rectal Injury
DVT & PE

Types of chemotherapy
• Adjuvant
Time → after surgery
Rational → treat residual disease [+ve Margin & +ve LN]
• Neoadjuvant (For T3-T4 Stages)
Time → before surgery
Rational → downstaging
 Urinary Diversions
Indications
(1) Radical cystectomy:
-Invasive T2-T3 bladder cancer.
-Uncontrollable T1 Tis bladder cancer. Danger Bladder
-No metastasis.
-Fit patient.

(2) Benign Diseases:

a) Exstrophy-Epispadias complex [Ectopia Vesica] Absent Bladder
b) Contracted bladder.
c) Neuropathic bladder Useless Bladder
d) Incurable fistula, Irremovable obstruction

Methods of Urinary Diversion

Methods

Non-Continent1 Continent2
Ileal Loop Conduit
Colon conduit
Ureterocutaneoustomy

Orthotopica Cutaneousb Rectal

Ileal W Neobladder Ileocecal Pouch Ureterosigmoidostomy

0

‫للمعرفة فقط ال غير‬

1Noncontinent urinary diversion is performed by either directly anastomosing the ureters to the anterior abdominal
wall (cutaneous ureterostomy) or using a segment of bowel to the ant. abd wall for ostomy bag drainage.

Bowels most commonly used→ 15-25 cm of ileum or colon

2 Continent mean (Can evacuate urinary reservoir voluntary "on his own desire ") done by using Sphincter/Valve

Bowels most commonly used → ileum or combination of terminal ileum and ascending colon
a Orthotopic
diversion (ortho meaning correct, topic meaning of a place) = neobladder diversion
preserve normal pathway of urine
 Non-continent Urinary Continent Urinary Diversion
Diversion Orthotopic neobladders Ureterosigmoidostomy Cutaneous urinary diversion
High risk patients → renal and hepatic impairment The procedure of choice
Indication

-Fit patient with adequate renal

and hepatic func
-When urethra is maintained2
Mechanism
Continence

Anal sphincter
No Continence External urethral sphincter the ileo-cecal valve

-An isolated vascularized loop of ileum -ileal segment is reconfigured as -Ureters are anastomosed to A continence mechanism as the ileo-
Technique

- Cutaneous non-continent stoma. a sphere the sigmoid colon with cecal valve is anastomosed to the skin
- Ureters anastomosed to the loop -anastomosed to membranous antireflux techniques3 as a stoma
- Urine is collected in a plastic bag urethra &both ureters [Inserted Submucosal] Emptying of urine is achieved by self-
-Urine and feces are mixed catheterization → Clean intermittent
leading to highest complication catheterization [CIC]
rate4
1-Ileal loop conduit -W-neobladder
Least intraoperative &immediate postoperative -Urethral Kock
Examples

Complications -Studer pouch

2-Colon1 conduit
Used in patient e' Hx pf Pelvic irradiation
(As Cervical Carcinoma in ♀)
3-Ureterocutaneoustomy
1 Transverse colon away from pelvis as any irradiated Organ has bad blood supply
2 not used in Tm Extending into Urethra or Hx of Urine incontinence d2 Sphincteric dysfunction [in Diabetic neuropathy & Spinal injury]
3 ↓↓ Rate of reflux of ascending infection of E-Coli so prevent recurrent aggressive pyelonephritis
4 Long standing mixing urine & Feces →Produce Nitic oxide (Strong Carcinogenic) → Sigmoid adenocarcinoma

So Bleeding per rectum & Hx of Urinary diversion → Don't treat as pile before exclusion Sigmoid adenocarcinoma by proctoscope
Complications
►Surgical related complications
1-Bleeding
2-Infection
3-Thromboembolism
4-Stricture
5-Leakage
►Nonsurgical related complications
●Metabolic
Hyperchloremic metabolic acidosis:
-It is seen when ileum or colon are used
- More common in patients with renal damage
-Urea is digested by bacteria and converted to ammonia.
Ammonium chloride absorption leads to hyperchloremic acidosis*
-In contrast, the use of gastric segments leads to hypochloremic alkalosis*
HCL Loss → Hematuria Urinary syndrome & Hypochloremic alkalosis
Symptoms
Acute acidosis →Thirst, anorexia nausea vomiting, weight loss, weakness, confusion, coma.
Chronic acidosis → bone demineralization [Pathological Fx]
Treatment
-Drainage of urine Source ‫للقضاء على‬
-IV infusion of alkaline agent e.g. sodium bicarbonate.
-ABx Source ‫للقضاء على‬
Ureterosigmoidostomy should be avoided.
Prevnetion
alkaline agent [sodium bicarbonate] ‫فوار فروت‬ ‫مرات يوميا‬3 ‫مش للهضم ده للميتابولزم‬
●Urinary
Urinary obstruction, infection, stone formation and renal failure
●Intestinal
a) Nutritional deficits and malabsorption /VitB12 Deficiency d2 terminal ileum removal
b) Adenocarcinoma of the colon
● Stomal problems.

* Hypochloremic alkalosis [lead to death, difficult to treat] dangerous than Hyperchloremic acidosis [Coma]
 Comparison of Bladder Cancers in Egypt and Western Countries
Feature Egypt West
Mean age 55 years 65
-Conventional
Etiology Smoking
-Bilharzial
Conventional Bilharzial
Symptoms Hematuria
Hematuria Dysuria,Frequency
Pathologic types
TCC 66% 90%
SCC 28% 5%
Adenocarcinoma 6% 2%
Undifferentiated - 2%
Morphology Fungating Papillary
75% of TCC are Ta-T1
Tumor stage
All non-TCC (SCC and Adenoca) are T2- T4
Main ttt Radical cystectomy + diversion TURBT+BCG

Tumors of the Renal pelvis & Ureter [Upper urothelial Tm]

- Calices, renal pelvis, and ureters are lined by a single continuous membrane of transitional epithelium.
- Development of malignancy in any part indicates that all other areas are at risk, so the entire urothelium should be
surveyed.
- Patients with an upper urothelial tumor have
up to 50% likelihood of developing TCC of the bladder & 2- 4 % chance of contralateral upper tract tumor.
- Patients with bladder cancer have
5% incidence of developing an upper tract tumor

Etiology Balkan nephropathy, phenacetin abuse, cigarette smoking

Symptoms Hematuria with occasional flank pain
Investigations
1. Cytology →helpful in high-grade lesions
2. IVU → radiolucent filling defects
3. Retrograde uretero- pyelography →filling defects.
4. Ureteroscopy & biopsy→ extremely accurate [Diagnostic]
5. CT scan →distinguishes radiolucent stones from soft tissue filling defects
differentiates between renal & TCC tumors of pelvis.
Treatment
- Nephroureterectomy with excision of a cuff of bladder
- Regular follow-up cystoscopy → d2 50% Risk of develop bladder cancer