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في ع

احلمد هللا على توفيقه وامتنانه، وعظيم نعمه وتتابع إحسانه، وأشهد أن ال إله إال اهللا وحده ال شريك له، وأشهد أن حممدا

تكون أيسر يف ؛ لتخرج يف أحسن صورة وأخصر عبارة، و

العماد األصفهاين، معتذرا : هـ إىل 596القاضي الفاضل البيساين عبد الرحيم املتوىف سنة

إنه قد وقع يل شيء، وما أدري أوقع لك أو ال، وها أنا أخربك به، وذلك أنين رأيت أنه ال يكتب إنسان كتابا يف يومه إال ن أحسن، لو زيد هذا لكان يستحسن، ولو قدم هذا لكان أفضل، ولو ترك هذا لكان

.انتهى

.فعلى من وجد عيبا أو نقصا أن ال يتأخر عن اإلرشاد والبيان، وله من اهللا األجر واملثوبة .، وهو سبحانه ويل اهلداية والتوفيق

1431شعبان 21 االثننيوكان االنتهاء منه يوم

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بسم اهللا الرمحن الرحيم


.اللهم صل وسلم عليه وعلى آله وأصحابه ومن تبعهم بإحسان إىل يوم لقائه

؛ لتخرج يف أحسن صورة وأخصر عبارة، ولكتاب جراحة املسالكفهذه ورقات خمتصرة، مجعتها تنظيما وترتيبا

القاضي الفاضل البيساين عبد الرحيم املتوىف سنة هكتب هذا وإين ال أكاد أنسى ما :عن كالم استدركه عليه

إنه قد وقع يل شيء، وما أدري أوقع لك أو ال، وها أنا أخربك به، وذلك أنين رأيت أنه ال يكتب إنسان كتابا يف يومه إال ن أحسن، لو زيد هذا لكان يستحسن، ولو قدم هذا لكان أفضل، ولو ترك هذا لكان لو غري هذا املكان لكا

انتهى)) ، وهذا من أعظم العرب، وهو دليل على استيالء النقص على مجلة البشر

فعلى من وجد عيبا أو نقصا أن ال يتأخر عن اإلرشاد والبيان، وله من اهللا األجر واملثوبة، وهو سبحانه ويل اهلداية والتوفيقطالب، وأن تكون عونا لكل تعاىل أن ينفع ذه الورقات

وكان االنتهاء منه يوم

[email protected]

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.ورسولهعبده اللهم صل وسلم عليه وعلى آله وأصحابه ومن تبعهم بإحسان إىل يوم لقائه

..أما بعد

فهذه ورقات خمتصرة، مجعتها تنظيما وترتيبا .احلفظ واملذاكرة

هذا وإين ال أكاد أنسى ماعن كالم استدركه عليه

إنه قد وقع يل شيء، وما أدري أوقع لك أو ال، وها أنا أخربك به، وذلك أنين رأيت أنه ال يكتب إنسان كتابا يف يومه إال ((لو غري هذا املكان لكا: "قال يف غده

، وهذا من أعظم العرب، وهو دليل على استيالء النقص على مجلة البشر"أمجل

فعلى من وجد عيبا أو نقصا أن ال يتأخر عن اإلرشاد والبيان، وله من اهللا األجر واملثوبة وإين ألرجو من اهللا

mailto:[email protected]

mailto:[email protected]

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ABBREVIATIONS

3DRT 3-D Radiation Therapy.

BC Bladder Cancer. BCG Bacillus Calmette-Guerin. BM Basement Membrane. BOO Bladder Outlet Obstruction.

C&S Culture & Sensitivity. CIS Carcinoma In Situ. CO Cardiac Out-put. CT Connective Tissue. CT Computerized Tomo-graphy.

ECSI Extra-Cytoplasmic Sperm Injection. ED Erectile Dys-function. EPS Expressed Prostatic Secretions. ESRD End-Stage Renal Disease.

ESWL Extra-corporeal Shock Wave Litho-tripsy.

FB Foreign Body.

GU Genito-Urinary. GFR Glomerular Filtration Rate.

HIFU High Intensity Focused US.

IBT Immuno-Bead Test. IVC Inferior Vena Cava. IVU Intra-Venous Uro-graphy.

KUB Kidneys, Ureters & Bladder X-ray.

LNs Lymph Nodes. LUTS Lower Urinary Tract Symptoms (dysuria, urgency & frequency).

MRI Magnetic Resonance Imaging.

N-V Neuro-Vascular. NHT Neo-adjuvant Hormonal Therapy. NOA Non-Obstructive Azoo-spermia.

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OAT syndrome

Oligo-zoo-spermia, Astheno-zoo-spermia & Terato-zoo-spermia.

PC Prostate Cancer. PCN Per-Cutaneous Nephrostomy. PCTs Proximal Convoluted Tubules. PSA Prostatic specific antigen.

RCC Renal Cell Carcinoma. RTA Renal Tubular Acidosis.

SCC Squamous Cell Carcinoma. STD Sexually Transmitted Diseases.

TCC Transitional Cell Carcinoma. TRUS Trans-Rectal Ultra-Sono-graphy. TUIP Trans-Urethral incision of the Prostate. TUNA Trans-Urethral Needle Ablation.

TURP Trans-Urethral Resection of the Prostate. TVT tension-free Trans-Vaginal Tape.

UDT Un-Descended Testis. UPJ Uretero-Pelvic Junction. US Ultra-Sono-graphy. UT Urinary Tract.

UTI Urinary Tract Infection. UTIs Urinary Tract Infections.

UVJ Uretero-Vesical Junction.

VCUG Voiding Cysto-Urethro-Gram.

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INDEX v Congenital anomalies of the genito-urinary tract (7) ..………………………………………….. o Renal anomalies ……………………………………………………………………………………………………………… o Ureteral anomalies …………………………………………………………………………………………………………. o Bladder & urethral anomalies …………………………………………………………………………………………. o Penis anomalies ………………………………………………………………………………………………………………. o Un-Descended Testis (UDT) ………………………………………………………………………………………………

6 7 8 11 12 13

v Trauma of the genito-urinary tract (4) …………………………………………………………………. 14 v Urinary Tract Infection (11) ………………………………………………………………………………… o GU tuberculosis ………………………………………………………………………………………………………………. o GU schistosomiasis …………………………………………………………………………………………………………. o Prostatitis ……………………………………………………………………………………………………………………….. o Epididymitis & epididymo-orchitis …………………………………………………………………………………..

19 24 26 28 30

v Tumors of the urinary tract (17) …………………………………………………………………………… o Tumors of the upper UT ………………………………………………………………………………………………….. o Bladder cancer ………………………………………………………………………………………………………………… o Prostate cancer ……………………………………………………………………………………………………………….. o Testicular Tumors ……………………………………………………………………………………………………………. o Differential diagnosis ……………………………………………………………………………………………………….

31 32 36 41 46 47

v Obstructive Uropathy (8) …………………………………………………………………………………….. o Urinary Stones ………………………………………………………………………………………………………………… § Renal Stones …………………………………………………………………………………………………………………… § Ureteral stones ……………………………………………………………………………………………………………….. § Bladder & prostatic stones ………………………………………………………………………………………………. v Benign Prostatic Hyper-plasIa (BPH) (5) ………………………………………………………………..

49 52 53 56 57 58

v Urinary Incontinence (6) ……………………………………………………………………………………… 63 v Andrology (4) ………………………………………………………………………………………………………. § Male infertility ……………………………………………………………………………………………………………….. § Erectile Dys-function (ED) ………………………………………………………………………………………………..

70 71 73

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CONGENITAL ANOMALIES OF

THE GENITO-URINARY TRACT

فضائل اجلهاد واالستشهاد يف سبيل اهللامن :)صلى الله عليه وسلم( الله رسول فقال ؟أفضل الناس أي !الله رسول يا :قيل: قال )رضي الله عنه( عن أيب سعيد اخلدري

))نمؤم داهجي يبيل فس الله فسهبن هالمو(( قالوا: ثم نقال ؟م: ))نمؤي مب فعش ناب معي الشقتي الله عديو اسالن نم هرش.((

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RENAL ANOMALIES 1. Anomalies of number: • Agenesis is the absence of renal tissue. • Absence of the ipsi-lateral hemi-trigone is diagnostic of unilateral renal agenesis. 2. Anomalies of rotation: o Persistent anterior position of the renal pelvis is the most common type & may be unilateral or

bilateral. 3. Anomalies of position (ectopic kidney): o Pelvic kidney is the most common type lying extra-peritoneally in the iliac fossa. • Incidence: § 1/1000. § More common in males on the left side.

o Thoracic kidney is extremely rare, more common in males on the left side. o Crossed renal ectopia with the crossed kidney lying inferiorly.

The ureteral orifices are located normally. 4. Anomalies of fusion: o Horseshoe kidney is the most common type with 90% fused at the lower poles by an isthmus

passing in front of the aorta, just below the origin of the inferior mesenteric artery at the level of L4. Patients may be asymptomatic (1/3) or present with symptoms of hydro-nephrosis (UPJ obstruction), infection or stones.

5. Renal dys-plasia: • It is a form of abnormal renal morphogenesis characterized histologically by primitive ducts &

cartilage. 6. Renal Cystic Diseases: • Most renal cysts are congenital & arise from dilated obstructed collecting ducts.

1) Autosomal recessive (infantile) polycystic kidney disease: o It is rare with no sex predilection. o The kidneys contain multiple tiny cysts so their shape is preserved. o It is characterized by hypertension, pulmonary hypo-plasia & portal fibrosis.

2) Autosomal dominant (adult) polycystic kidney disease: o It is the most common type of renal cystic diseases & is responsible for 10% of end-stage renal

disease (ESRD). o It is an inherited autosomal dominant single gene (chromosome 16q) disease with 100% penetrance. o The kidneys contain multiple cysts of variable size so their shape is distorted. o It is characterized by diffuse bilateral progressive cystic degeneration of the kidneys, flank masses,

hypertension, renal failure & death around the age of 50.

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o The best diagnostic tool is the US or CT scan. o Treatment: § Medical treatment of renal failure. § Dialysis or renal transplantation.

3) Medullary Sponge Kidney: o It is a congenital deformity of the renal medulla characterized by dilated collecting ducts. o Its course & progression are benign, however it predisposes to calcium phosphate nephro-lithiasis in

adults. 7. Simple (Retention) cyst: • It is the most common cystic lesion of the kidney. • It may be solitary or multiple, unilateral or bilateral. • Clinical picture: § Asymptomatic (discovered accidentally during routine US, CT scan or IVU). § Abdominal mass.

• Treatment is seldom required.

URETERAL ANOMALIES 1. Uretero-Pelvic Junction (UPJ) obstruction: • Indidence:

o More common in males (2:1). • Etiology:

1. Intrinsic lesion of the circular smooth muscle of the UPJ (adynamic segment). 2. Valvular mucosal folds. 3. Extrinsic compression by an aberrant, accessory or early branching vessel to the lower pole.

• Diagnosis:

1. Intra-uterine US. 2. IVU shows Hydro-nephrosis with abrupt cut off at the UPJ. 3. Radio-active isotope study (reno-gram).

• Treatment:

1. Open or laparoscopic pyelo-plasty (the gold standard treatment). 2. Endo-pyelo-tomy “endoscopic incision of the tight UPJ” (the 1st line treatment in many centers). 3. Nephrectomy if < 10% of renal function remains.

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2. Vesico-Ureteral Reflux (VUR): • It is the backward flow of urine from the bladder into the upper UT. • It is associated with recurrent UTIs & renal damage (reflux nephro-pathy) which may result in

hypertension or ESRD. • Types:

1. 1ry (1% of children, 5 times more common in girls & with family history). 2. 2ry to a neurogenic bladder.

• Pathology: Abnormal UVJ. • Etiology:

1. A short submucosal ureter. 2. Lateral placement of the ureteral orifice. 3. Abnormal configuration of the ureteral orifice (stadium, horseshoe or golf hole) 4. Infection.

• Grading:

According to the radiographic appearance on VCUG: Ø Grade I: Reflux into ureter without dilation. Ø Grade II: Reflux into pelvis & calyces without dilation. Ø Grade III: Mild to moderate dilatation of ureter & pelvis. Ø Grade IV: Moderate dilatation &/or tortuosity of ureter. Ø Grade V: Severe dilation & tortuosity of ureter, pelvis, & calyces. • Diagnosis:

o The commonest presentation is a child with UTI. o The best diagnostic tool is the VCUG.

• Treatment:

o Medical: For infants & young children with mild to moderate reflux (grades I-III).

1. Regular timed voiding. 2. Continuous low dose antibiotic prophylaxis. 3. Regular urine cultures (every 3 months). 4. Regular VCUG & renal US (every year).

o Surgical:

For: § Breakthrough infection despite antibiotic prophylaxis § Progressive renal scarring & damage despite antibiotic prophylaxis. § Severe reflux (grades IV & V).

1. Ureteral re-implantation (success rate > 90% in experienced hands). 2. Endoscopic sub-trigonal injection of the ureteral orifice (has inferior results).

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3. Ureteral duplication: • Incidence:

o It is the most common anomaly of the ureter. o More common in females (2:1).

• It ranges from a bifid pelvis to a complete duplex system with two ureters opening with two ureteral

orifices in the bladder. • The ureteral orifice of the upper renal segment drains inferiorly & medially to the orifice of the

lower segment (Meyer-Weigert law). • The orifice of the upper segment is prone to the development of uretero-cele (often obstructed)

while the orifice of the lower segment is prone to reflux. • Diagnosis:

o Patients may be asymptomatic or present with UTI. o The best diagnostic tool is the IVU.

• Treatment:

1. Ureteral re-implantation for reflex. 2. Endoscopic incision for uretero-cele.

4. Ectopic ureter: • 80% are associated with a duplicated system (more common in females). • 20% are single with an absent hemitrigone (more common in males). • Most common sites for insertion:

o In females: The urethra, vestibule & vagina (present with urinary incontinence). o In males: The posterior urethra & seminal vesicles (present with UTI “late”).

5. Uretero-cele: • It is a congenital cystic ballooning of the terminal submucosal ureter (mostly 2ry to stenotic ureteral

orifice). • Types:

1. Simple. 2. Ectopic.

• Diagnosis:

1. Prenatal US. 2. IVU (cysto-gram phase) shows a characteristic cobra head or spring onion deformity. 3. VCUG shows reflux (40%). 4. Cysto-scopy (confirmative).

• Treatment:

o Endoscopic trans-urethral incision of the uretero-cele allowing drainage.

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BLADDER & URETHRAL ANOMALIES v Exstrophy Complex: • It is a rare congenital defect due to persistence of the cloacal membrane in utero. • Incidence:

o 1/30.000. o More common in males (3:1).

• Types:

According to the severity of the defect: 1. Cloacal Exstrophy (10%): o It presents by a massive defect of the anterior abdominal wall, exposed bladder, ileo-cecal bowel &

a short blind-ending colonic segment with imperforate anus. o It may be associated with myelo-meningo-cele (50%). 2. Classical Bladder Exstrophy (60%): o It presents by a protruding red mass in the supra-pubic region (the exposed posterior wall & trigone

of the bladder) & epi-spadias. o It may be associated with a wide separation of the symphysis pubis & lower rectus muscles. o Treatment:

Staged functional reconstruction, preferably in the 1st 48 hours of life (to minimize bladder damage due to environmental exposure).

3. Epi-spadias (30%): o It presents by an abnormal urethral opening on the dorsum of the penis or clitoris. o It may be associated with a lesser degree of separation of the symphysis pubis. v Posterior urethral valves: • They are the most common cause of bladder outlet obstruction in boys. • They are congenital membrane-like structures located in the distal prostatic urethra & covered by

transitional epithelium. • Incidence:

o 1/8000 male births. • Diagnosis:

o They present with variable degrees of obstruction & usually diagnosed within the 1st year of life. o VCUG shows a dilated & elongated posterior urethra & reflux (50%). o US. o Renal scan. o Cysto-urethro-scopy (note bladder trabeculation).

• Treatment:

o Endoscopic resection of the valves.

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PENIS ANOMALIES v Hypo-spadias: • It is the most common anomaly of the penis resulting from incomplete development of the anterior

urethra. • Incidence:

o 1/300 male births.

o 7% have a father with hypo-spadias. o 14% have a brother with hypo-spadias. o 21% have a 2nd family member with hypo-spadias.

• Etiology:

o Multi-factorial genetic inheritance. • Clinical picture:

o An abnormal urethral opening (proximal to its normal location) on the ventral surface of the penis.

o Ventral chordee or curvature of the penis. o Absence of the ventral part of the prepuce.

• Classification:

According to: o The meatal position (glanular & coronal (75%), distal, mid or proximal shaft, peno-scrotal &

perineal). o The degree of chordee (mild, moderate & severe), it ↑ with more proximal meatal position.

• Associated Anomalies:

o UDT (25%). o Inguinal hernia (10%). o Upper UT anomalies (renal agenesis, ureteral duplication, …) (5%). o Intersex (with severe forms of hypo-spadias & ambiguous genitalia or bilateral non-palpable

testis). • Treatment:

o There are > 100 surgical procedures & all must contend with functional & plastic repair of the urethra & correction of chordee.

o The optimal time for repair is before school age, but avoid the 1st 1-2 years for fear of dissociation anxiety of the child.

o Surgical complications include failure, urethra-cutaneous fistula, persistent chordee, urethral stricture, diverticula & meatal stenosis.

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UN-DESCENDED TESTIS (UDT) • Incidence:

o 3% of full-term infants. o 30% of pre-mature infants. o Most of these testes descend spontaneously by the age of 1 year leaving a true incidence of

about 1%. o 10% are bilateral (3% of which have one or both testes absent).

• Etiology: may be related to:

o Abnormal development of the gubernaculum & epididymis. o Fetal androgen levels.

• Significance:

o 10% of testicular cancer arise in UDT (60% are seminoma). o Infertility (30% only with bilateral cryptorchidism will be fertile). o Inguinal hernia (25%) o Torsion.

• Classification:

o On the posterior abdominal wall (cryptorchidism). o Intra-abdominal (10%), proximal to the internal ring. o Intra-canalicular in the inguinal canal (65%, of which 80% are palpable). o Ectopic: In the superficial inguinal pouch, perineum, femoral canal, supra-pubic region or the

contra-lateral scrotal compartment (rare). • Diagnosis:

o Carefully palpate areas of mal-descent & ectopic areas. o A non palpable testis is either intra-abdominal, inguinal, ectopic or absent (further investigated

by US, CT scan, laparoscopy or surgical exploration). • Differential diagnosis: Retractile testis:

o It can be easily brought down into the scrotum when the child is squatting or under anesthesia (treatment is not required).

• Treatment: The optimal time for surgery is about the age of 1 year, aiming at:

1. ↓ risk of malignancy. 2. ↓ risk of torsion. 3. Improve prospects of fertility. 4. Repair of the associated hernia. 5. Avoid psycological problems.

o Hormonal: GnRH or HCG in bilateral UDT (success rate up to 70% & 50% respectively).

It is contraindicated in ectopic testes, hernia & after prior orchiopexy.

o Surigcal: Orchiopexy: Adequate mobilization, repair of the associated hernia & fixation of the testis in sub-dartos pouch.

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TRAUMA OF

THE GENITO-URINARY TRACT

فضائل اجلهاد واالستشهاد يف سبيل اهللامن ،الجهاد يعدل عمل على دلني :فقال )صلى الله عليه وسلم( الله رسول إلى رجل جاء: قال )رضي الله عنه( عن أيب هريرة

ومن :قال ،))تفطر ولا وتصوم ،تفتر ولا فتقوم مسجدك تدخل أن المجاهد خرج إذا تستطيع هل(( :قال ،))أجده لا(( :قاليعطتسي ك؟ذل.!

.حسنات له فيكتب طوله في ليستن المجاهد فرس إن :هريرة أبو قال

RENAL TRAUMA URETERAL TRAUMA BLADDER TRAUMA URETHRAL TRAUMA TRAUMA Ant. ureth. injury Post. ureth. injury

1. Penetrating (gunshot or stab wounds). 2. Blunt (pedestrian struck, motor vehicle accidents, sports or

falls) (80-90%). 3. Iatrogenic (endo-urologic procedures or ESWL).

1. … 2. … (deceleration

injury causing avulsion of UPJ).

3. … (during pelvic surgery e.g. hysterectomy or uretero-scopic).

1. … 2. … (sever trauma to

the lower abdomen).

زي اللي قبله .… .34. Fracture pelvis.

• … (straddle falls

crushing the urethra against the pubic bones).

• Fracture pelvis

(motor vehicle accidents).

DIAGNOSIS PHYSICAL EXAMINATION

• Ecchymosis of the flank, fracture rib or stab wound.

INVESTIGATIONS LABORATORY

• Urine analysis: Haematuria is the hallmark of renal injury (although its degree does not correlate with the extent of injury).

RADIOLOGICAL

• CT scan: o For accurate diagnosis & grading in stable patients. o It is both sensitive & specific for demonstrating:

1. Parenchymal laceration. 2. Segmental parenchymal infarcts. 3. Urinary extravasation. 4. Size & location of retro-peritoneal hematoma. 5. Associated intra-abdominal injuries (spleen, liver or bowel).

• IVU: o For assessment of gross function & evaluation of the uninjured

kidney in haemo-dynamically unstable patients. • US: o Not recommended as an initial study as it does not assess the

function. • Radio-nuclide renal scinti-graphy: o Documenting the presence of a functioning kidney in patients

with a contraindication for iodinated contrast material.

v Penetrating injury:

• Haematuria (80%). • IVU may or may

not be diagnostic. v Retrograde Pyelo-

graphy detects the injury.

v Iatrogenic

injury: • Flank pain, fever &

paralytic ileus following intra- abdominal or pelvic surgery.

• CT & IVU show delayed excretion, hydro-nephrosis & extravasation.

• Ascending cysto-graphy:

o Extra-peritoneal

rupture: § Extravasation of

contrast material into the pelvis & retro-peritoneum.

o Intra-peritoneal

rupture: § Extravasation of

contrast material into the peritoneal cavity outlining loops of small intestine.

• History of perineal trauma followed by perineal pain & inability to void.

• If Buck's fascia is

not ruptured, ecchymosis will be limited to the penis.

• If ruptured,

ecchymosis will be limited to Colle's fascia in the perineum & Scorpa's fascia in the abdomen (butterfly ecchymosis).

SYMPTOMS • Suspected fracture

pelvis & inability to void.

• Bloody urethral discharge.

PHYSICAL

EXAMINATION • Abdominal: Supra-

pubic fullness or dullness due to pelvic hematoma (due to rupture of the peri-prostatic venous plexus).

• DRE: Boggy

indistinct mass indicating that the prostate is displaced upwards.

CLASSIFICATION • GRADE I: o Contusion or confined sub-capsular hematoma without

parenchymal laceration. • GRADE II: o Confined peri-renal hematoma. Or o Cortical laceration < 1 cm deep without urinary extravasation

(simple laceration). • GRADE III: o Cortical laceration > 1 cm deep without urinary extravasation. • GRADE IV: o Parenchymal laceration extending through the cortico-

medullary junction & the collecting system with urinary extravasation.

• GRADE V: o Multiple lacerations & main renal artery thrombosis.

BLADDER TRAUMA 1. Contusion: o Injury to the bladder wall with haematuria

& peri-vesical hematoma without extravasation.

2. Extra-peritoneal rupture: o Rupture of the lateral wall or floor of the

bladder leading to urinary extravasation into the pelvis & retro-peritoneum.

3. Intra-peritoneal rupture: o Rupture of the bladder dome (sever

trauma to the lower abdomen) leading to urinary extravasation into the peritoneal cavity.

1. Contusion: o Without urinary

extravasation. 2. Laceration: o With

extravasation.

RADIOLOGICAL • Retrograde

urethra-graphy: ü Should be

performed with the patient in 45o & the penis is stretched perpendicular over the ...

o Complete

urethral rupture: § Extravasation of

contrast material with no opacification of the bladder.

o Partial urethral rupture:

§ Extravasation of contrast material with partial opacification of the bladder.

CLASSIFICATION

1.Type I: o Stretch injury with

intact urethra. 2.Type II: o Partial tear with

some continuity. 3.Type III: o Complete tear with

no continuity.

TREATMENT • Indications of exploration: o Absolute: § external trauma with persistent renal bleeding. o Relative: 1. Non-viable tissue & major laceration. 2. Urinary extravasation (87% are cured spontaneously). 3. Concomitant laparotomy for associated injuries. 4. Penetrating trauma.

COMPLICATIONS • Early (within 4 weeks): 1. Urinary extravasation & urinoma formation (stent or

nephrostomy). 2. Sepsis & peri-nephric abscess (PC drainage). 3. Delayed bleeding. 4. A-V fistula & pseudo-aneurysm. 5. Hypertension. • Late (after 4 weeks): 1. Hydro-nephrosis. 2. Stone formation. 3. Chronic pyelo-nephritis. 4. Hypertension.

• Immediate recognition (within few days):

1. Exploration. 2. Lower ureteral

injuries: Ureteral re-implantation ± psoas hitch or boari bladder flap.

3. An internal stent is left until complete healing.

• Delayed

recognition: 1. Urinary diversion

by PCN & drainage of any urinary collection.

2. Reconstructive surgery when hydro-nephrosis & infection subside.

• Extra-peritoneal rupture:

o If minor trauma & no evidence of infected urine:

§ Urethral catheter. o If major trauma: § Explore & repair. • Intra-peritoneal

rupture: o Trans-peritoneal

exploration to rule out associated injuries & remove urine from the peritoneal cavity.

COMPLICATIONS

• Cystitis, sepsis &

pelvic collection. • Vesico-vaginal

fistula.

• Contusion: o If the patient can

void with mild haematuria: § Conservative

treatment. o If there is

significant haematuria: § Urethral catheter

for several days. • Laceration: o Supra-pubic

diversion with spontaneous healing.

• Stretch injury & partial tear:

o Urethral catheter for few days.

• Complete tear: 1.1ry realignment: § Opposition of the

torn ends of the urethra over a catheter with concomitant supra-pubic diversion.

2.Supra-pubic

diversion with delayed repair.

3.Endo-urologic: § May allow 1ry

alignment without the risk of exploration of the disrupted urethra.

PENILE TRUMA SCROTAL TRUMA TESTICULAR TRUMA • More common in young age (15- 40 years).

TRAUMA 1. Penetrating (gunshot or stab wounds). 2. Machinery accidents (partial or complete

avulsion of genital skin). 3. Animal attacks. 4. Self mutilation. 5. Spontaneous penile rupture:

May occur during sexual intercourse & result in rupture of tunica albuginea of the corpora.

1. … 2. Blunt.

1. … 2. Blunt (the most common cause) (motor vehicle

accidents or straddle falls). 3. Spontaneous testicular rupture (with minimal

trauma).

DIAGNOSIS • Clinical picture of SPF: o Sharp onset pain, swelling & ecchymosis. o Deviation of the penis away from the side of

fracture with loss of erection.

• Physical examination: o Assess corporal integrity. o Look for blood at the meatus. • Retrograde urethro-graphy: o To exclude urethral injury.

• Physical examination. • Scrotal US.

TREATMENT 1. Penetrating trauma:

Debridement, haemostasis & repair of injured tissue.

2. Machinery accidents:

Debridement & skin grafting. 3. Spontaneous penile rupture:

Explore & repair tunica albuginea with non absorbable suture. If there is concomitant urethral injury: Urethral catheter.

• Explore with debridement & 1ry repair. • Minor trauma: o Explore & repair the testis if possible. • If the testis is severely injured: o Orchidectomy.

19


URINARY TRACT INFECTION

فضائل اجلهاد واالستشهاد يف سبيل اهللامن نس عن أنب كالم )هنع الله يضر( نع بيالن )لمسو هليع لى اللهة(( :قال )صودي لغبيل فس الله ة أوحور ريخ نا مينا الدمو به يحدث ولم يغز ولم مات من: (()صلى الله عليه وسلم( الله رسول قال: قال )رضي الله عنه( هريرة أبي عنو)) فيهاهفسن اتلى مع ةبعش ننفاق م.((

20


URINARY TRACT INFECTION v Types: • Non specific. • Specific:

o Bacterial e.g. TB. o Fungal e.g. Actinomycosis. o Parasitic e.g. Bilharziasis.

v Definitions: • Bacteruria: The presence of bacteria in urine. • Pyuria : The presence of > 5 pus cells /HPF. v Causative organisms: 1. E-coli “aerobic gram -ve” (the most common). 2. Certain gram +ve cocci (entero-cocci). 3. Chlamydia trachomatis “needs certain culture techniques”. v Classification: • 1st infection. • Recurrent infection:

o Un-resolved bacteruria. o Bacterial persistence. o Re-infection.

v Diagnosis: • Urine collection:

1. Adult males: Clean mid stream sample: urethral meatus is cleansed with betadine (especially in non-circumcised males), first 30 ml is discarded & next 50-100 ml is collected & examined as soon as possible.

2. Adult females: Clean midstream sample as in males. If not satisfactory, get the sample by catheterization under complete aseptic technique.

3. Children: Sterile plastic bag over the penis or vulva after their sterilization. If not reliable, get the sample by supra pubic needle aspiration of the bladder.

• Urine analysis:

o Microscopic examination: § Infection: Pus cells (WBCs) > 5/HPF. § Haematuria: RBCs > 5/HPF. § Microorganisms: bacterial count > 105 colony forming unit/ml.

o Chemical examination: § Nitrites: bacteria reduce nitrates into nitrites. § Leukocyte esterase produced by pus cells.

• Urine culture.

21

ACUTE PYELO-NEPHRITIS

CHRONIC PYELO-NEPHRITIS PYO-NEPHROSIS PERI-NEPHRIC

ABCESS RENAL ABSCESS

(CARBUNCLE) ACUTE CYSTITIS CHRONIC CYSTITIS DE

FINITI

ON

• Bacterial infection causing inflammation of the renal pelvis & parenchyma.

• It is a process of renal scarring resulting in renal insufficiency.

• It accounts for 18% of adult cases & 30% of childhood cases of renal failure.

• Hydro-nephrosis associated with suppurative destruction of the renal parenchyma resulting in nearly total loss of renal function.

• It is a collection of pus around the kidney.

• It is a collection of pus confined to the renal parenchyma.

• More common in females.

• The ascending route is the 1ry mode of infection.

• It may be due to bacterial persistence or re-infection.

CO • E-coli (80%). • E-coli (60%).

PRED

. FAC

TORS

1. Obstruction (stones or stricture).

2. VUR. 3. Septic focus. 4. Instrumentation.

1. … 2. … 3. DM. 4. Analgesic

nephropathy.

1. … 2. UTI. 3. Surgery.

1. … 2. … 3. DM. 4. Skin carbuncle. 5. Neuro-genic

bladder (VUR). 6. IV drug abuse. 7. Haemo-dialysis.

1. … 2. Diverticulum. 3. Fistula.

CLIN

ICAL

PICT

URE

1. Patient looks ill. 2. High grade fever,

tachycardia & chills.

3. Nausea, vomiting & malaise.

4. Flank pain &

tenderness. 5. Tender renal

angle. 6. LUTS.

o Patients may be asymptomatic or present with:

• Hypertension. • Symptoms of

renal failure.

1. … 2. Fever, tachycardia

& chills. 3. … 4. … 5. …

o As in pyo-nephrosis.

1. … 2. Fever,

tachycardia & chills.

3. … 4. … 5. …

o LUTS. o Supra-pubic pain.

22

INVESTIGATIONS LABORATORY

Uri

ne

• Pyruia, bacterurea & haematurea.

• Pyuria, bacterurea & proteinurea.

• pyurai & bacterurea (except in completely obstructed cases).

• Pyuria, bacterurea & haematurea.

• Pyuria & bacterurea.

Blo

od • Leukocytosis.

• High blood urea & serum creatinine in bilateral cases.

• High blood urea &

serum creatinine.

• Urine C&S. • Urine C&S.

RADIOLOGICAL

US

& K

UB

• Detects the presence of obstruction.

• Small sized kidney with irregular outlines.

• Dilated collecting system with dependent echoes.

• Detects the presence of obstruction (rarely indicated in uncomplicated cases).

IVU

• Detects the cause of infection (e.g. stones)

• Small atrophic kidney.

• Impaired excretion of contrast material.

• Disturbed arrangement of the calyces.

• Non-visualized kidney.

• Radio-nucleotide imaging with gallium 67 (differentiates it from tumors).

• IVU & ascending cystogram detects VUR & vesico-vaginal fistula.

VCU

G • Detects VUR

(after resolution of acute stage).

• Detects VUR.

CT

• Suppurative destruction of the renal parenchyma.

• It is the best diagnostic tool. (differentiates it from pyo-nephrosis).

23

COMP

LICAO

NS 1. Peri-nephric or

renal abcess. 2. Renal

insufficiency in bilateral cases.

MA

NAGE

MENT

1. Obstruction must be relieved by ureteral catheter or PCN.

2. Bed rest &

analgesics. 3. ↑ fluid intake,

oral or parentral (if there is vomiting).

4. Antibiotics (10-14

days): Ampicillin + gentamycin, fluroquinolones or 3rd generation chephalosporins.

• Correction of any underlying structural abnormality.

• Prevention the

recurrence of UTI by long term prophylactic antibiotics.

• unilateral atrophic

kidney: Nephrectomy.

• Nephrectomy. • Small abscess: Medical treatment (antibiotics) + follow up.

• Large abscess:

Surgical drainage.

• < 3 cm: Medical treatment (antibiotics) + follow up.

• 3-5 cm:

PC drainage. • > 5 cm:

Surgical drainage.

1. Bed rest & analgesics.

2. ↑ fluid intake. 3. Vaginal douching

with anti-septic solution.

4. Antibiotics:

Trimethoprim + sulfa-methoxazole, nitro-furantoin or fluro-quinolones.

24


GENITO-URINARY (RENAL) TUBERCULOSIS • It is a granulomatous lesion always 2ry to a 1ry focus in the lungs, bone, GIT or LNs. v Causative organism: o Mycobacterium tuberculosis (gram +ve, acid fast, alcohol fast & stained by Zeihl-Neilson stain). v Incidence: o 20-40 years. o More common in males. v Pathogenesis: o Renal TB usually starts at the cortex (haematogenous spread). v Pathological types: 1. Renal tubercle (Medley's focus). 2. Renal nodule or nodules without caseation. 3. Moth-eaten appearance of one or more minor calices due to papillary ulcers (the 1st radiological

sign). 4. Ulcero-cavernous (erosion connecting with the renal pelvis). 5. Hydro-nephrosis. 6. Pyo-nephrosis. 7. Auto-nephrectomy: Complete replacement by cheesy material & renal atrophy with PUJ

obstruction. 8. Milliary TB: bilateral in immuno-compromised patients & incompatible with life (seen only in post

mortem specimen).

• Fate: o Healing & scarring with fibrosis & calcification. o Progression & spread (softening, caseation & organ destruction with dystrophic calcification). o Encapsulation.

• Microscopic appearance: o The solid tubercle consists of: § A central collection of epithelioid cells in whorl formation & giant cells of Langhan's type. § Surrounded by lympho-cytes & plasma cells intermingled with fibro-blasts.

o The soft tubercle is similar but with predominance of central necrosis. v Clinical picture: 1. Asymptomatic. 2. Frequency of micturition (the most common & usually the 1st symptom).

It is due to highly acidic urine, polyuria, irritation of the bladder by caseous material, tuberculous cystitis, 2ry infection or contracted bladder.

3. Haematuria (occasionally the 1st symptom).

25


4. Dull aching pain in the loin or renal colic (rare) due to ureteral obstruction by caseous material or

blood clot. 5. Sterile pyuria. 6. Tuberculosis of epididymis, prostate or seminal vesicles may be present. 7. General symptoms in patients with active pulmonary lesions. v Investigations:

• Laboratory: o Urine analysis § Pyuria, haematuria & albuminurea. § Highly acidic urine.

o Tubercle bacilli can be identified by: § Acid fast staining of the sediment of 24-hour urine of 3 successive days. § Urine culture (Dorset egg or Lowenstein-Jensen medium). § Guinea pig inoculation.

• Radiological: 1. KUB shows enlarged kidney or punctate renal calcification. 2. US shows the size of the kidneys, stones, thickness of renal parenchyma & contents of pelvis &

calyces. 3. IVU shows:

o Moth-eaten appearance of one or more calyces due to papillary ulcers. o Abscess cavities connecting with the calyces. o Ureteral strictures (single or multiple) with 2ry dilatation. o Ureteral Straightening from shortening due to fibrosis.

v Treatment: • Medical (anti-tuberculous drugs):

Triple drug therapy from: § Isoniazid 300 mg/day. § Rifampin 600 mg/day. § Ethambutol 800 mg/day. § Pyrazinamide 1 gm/day. § Streptomycin IM 1 g/day for the 1st month then 1 g twice a week.

• Surgical:

Unilateral advanced disease: Nephro-ureter-ectomy.

26


GENITO-URINARY SCHISTOSOMIASIS v Incidence: o 300 million humans are infested. o Urinary involvement: 40-60%. v Causative organisms: o Schistosoma mansoni, japonicum & haematobium. o GU schistosomiasis is caused mainly by S. haematobium. o It is endemic in Africa & certain areas in the Middle East. o Intestinal schistosomiasis is caused mainly by S. mansoni & japonicum.

• Life cycle: 1. Humans are infested through contact with fresh water contaminated with the infective stage (larva

= cercaria) which penetrates the skin or mucous membrane. 2. Cercaria reaches the general circulation & only worms that reach the portal circulation live. 3. Urinary schistosoma reaches the sub-mucosal venous plexus in the bladder, ureter & seminal

vesicles. 4. Ova are eliminated in human faeces & urine. 5. If they reach fresh water, they start asexual cycle in snails & continue the life cycle. v Pathogenesis: Ø Stage 1:

Generalization or incubation period: § Larvas acquire host antigenic material as immunological camouflage & initiate hypersensitivity &

general manifestations of illness. § Clinical picture: Allergic skin reaction, fever, cough, malaise, bone aches & GIT symptoms. Ø Stage 2:

Deposition of ova by mature worm: § Toxins & antigenic materials initiate a granulomatous inflammatory reaction around the egg

(Bilharzial pseudo-tubercles). § Clinical picture:

1. General symptoms (Swimmer’s itch or Katayama fever). 2. GU symptoms (terminal painful haematuria, dysuria, pyuria & haemo-spermia “irritative LUTS”).

Ø Stage 3:

Late complications: § The end result of repeated chronic infestation & 2ry bacterial infection is fibrosis which involves the

bladder, ureter, urethra & seminal vesicles. § Lesions may be atrophic or hypertrophic as polyps, nodules, masses, tubercles, ulcers or sandy

patches (calcification).

27


v Complications: 1. Hydro-nephrosis & renal atrophy. 2. Contracted bladder. 3. Bladder cancer (usually SCC). v Investigations: • Diagnosis of infection: § Urine sediment shows terminal spined egg (S. Haematobium). § Rectal or bladder mucosal biopsy shows granuloma. § Seriological tests (Ag-Ab reaction) “not reliable”.

• Diagnosis of sequelae & complications: § KUB shows calcification of the bladder, distal ureter, urethra & seminal vesicles. § US & CT for polyps, obstructive & destructive lesions. § IVU for obstructive uropathy. § Endoscopy (diagnostic & therapeutic).

v Treatment: • Medical: § Praziquantel (Biltricide) 40 mg/Kg in a single oral dose (the drug of choice for all species). § Metrifonate 7.5-10 mg/Kg in 3 oral doses at 14 days Intervals (the drug of choice for endemic S.

Haematobium). § 3-Niridazole (Ambilhar) 25 mg/Kg/day in 2 divided doses for 5-7 days orally.

• Surgical:

For the lesion or the complication: § Polyp: Resection. § Ureteral stenosis: Ureteral dilatation or re-implantation. § Contracted bladder: Bladder augmentation. § Bladder cancer: Cystectomy with urinary diversion.

28


PROSTATITIS v Incidence: o It affects males at any age with a peak at sexual activity (20-40 years). v NIH classification: I. Acute bacterial prostatitis. II. Chronic bacterial prostatitis / recurrent infection. III. Chronic non-bacterial prostatitis / chronic pelvic pain syndrome (no detectable infection).

IIIA: Inflammatory: WBCs present in semen, expressed prostatic secretions (EPS) or urine. IIIB: Non-inflammatory: No WBCs in semen, EPS or urine.

VI. Asymptomatic inflammatory prostatitis: detected by presence of WBCs in EPS during evaluation for other disorders. v Etiology: o Acute bacterial prostatitis is due to reflux of infected urine into prostatic ducts that drain into

posterior urethra causing inflammation & edema that occlude these ducts, trapping bacteria within, leading to chronic bacterial prostatitis.

o Non-bacterial prostatitis is due to intra-prostatic reflux of urine causing chemical prostatitis. • Causative organisms: o E. coli (80%). o Othe gram -ve organisms (Pseudomonas, Serratia & Klebsiella) (10-15%). o Enterococci (5-10%). v Clinical picture: • Symptoms: o LUTS & malaise. o Pain in the perineum, groin, testes or supra-pubic region. • Signs: o Fever, tachycardia & chills (acute bacterial prostatitis). o ↓ urinary flow rate & nocturia. o DRE: tender, boggy or firm prostate. v Differential diagnosis: o Distal ureteral stone. o Urethral stricture. o BPH. o Seminal vesicle cyst. o Prostatic cyst.

29


v Investigations: • Laboratory: o C&S of:

ü Semen, EPS & urine o The 4 glass test (Meares-Stamey) (the gold standard for diagnosis of bacterial prostatitis):

After cleansing & retraction of the fore skin: ü The first 10 ml (urethral flora) is collected in a sterile container (VB 1). ü After voiding 200 ml, a clean mid-stream sample is collected in a sterile container (VB2)

“represents bladder, prostate or urethral bacteria”. ü The patient stops voiding & prostatic massage is performed & EPS are gently milked. ü The next 10 ml is collected in a sterile container (VB3) “represents prostatic infection”.

• Radiological: 1. Abdominal US for bladder scanning & post-voiding residual urine volume to ensure complete

bladder emptying. 2. TRUS. 3. Uro-flow-metry for patients with voiding complaints. v Treatment: • Acute bacterial prostatitis:

Antibiotics (trimethoprim + sulfa-methoxazole or fluro-quinolones) for 6-12 weeks. • Chronic bacterial prostatitis:

Antibiotics for extended periods. • Recurrent infection:

Long-term prophylactic antibiotics for 6 months. • Non-bacterial prostatitis:

§ IIIA: broad spectrum antibiotics, α-blockers, anti-inflammatory drugs, phyto-therapy & trans-urethral micro-wave therapy.

§ IIIB: α-blockers, analgesics, muscle relaxants & relaxation exercises.

30


EPIDIDYMITIS & EPIDIDYMO-ORCHITIS • Definition: Inflammation of the epididymis ± testis. • Incidence: More common in teenage with a peak at 32 years. • Causative organisms: o Gram -ve organisms. o STDs (Chlamydia, gonorrhea & ureaplasma). o 2ry to viral infection mainly with parotitis (teenage). • Clinical picture: o Usually gradual onset & unilateral. o Dull aching pain radiating to the spermatic cord, lower abdomen or flank. o Pain is relieved by scrotal elevation (Prehn's sign). o Swollen & tender epididymis ± testis. o Scrotal wall erythema. • Complications: o Abscess formation. o Testicular infarction. o Chronic pain. o Infertility. • Differential diagnosis:

TORSION INFLAMMATION Mode of onset • Abrupt. • Hours to days. Affected testis • Higher than opposite. • No change in position. Affected epididymis • Usually non-palpable. • Palpable & tender.

Urethral discharge • Absent. • Present. Cremasteric reflex • May be absent. • Usually present. Fever • Usually absent. • May be present.

Scrotal elevation (Prehn's sign) • No change in pain. • Pain is relieved. Scrotal duplex • ↓ blood flow. • ↑ blood flow. • Investigations: o Laboratory: Urine analysis & C&S. o Radiological: Scrotal duplex to differentiate between torsion & inflammation. • Treatment: 1. Bed rest & analgesics. 2. Scrotal elevation. 3. Antibiotics (erythromycin, fluro-quinolones or 3rd generation chephalosporins).

31


TUMORS OF

THE URINARY TRACT

فضائل اجلهاد واالستشهاد يف سبيل اهللامن نس عن أنب كالم )هنع الله يضر( أن بيالن )لمسو هليع لى اللها(( :قال )صم نم دل أحخدة ينالج بحأن ي جعرإلى ي

)).الكرامة من يرى لما مرات عشر فيقتل يرجع أن يتمنى فإنه ،الشهيد غير شيء من الأرض على ما له وأن الدنيا

32


TUMORS OF THE UPPER UT v Benign:

1. Renal cortical adenoma. 2. Renal onco-cytoma. 3. Angio-myo-lipoma (hamartoma) “rare”.

v Malignant: • 1ry:

1. RCC. 2. Wilm's tumor (Nephro-blastoma). 3. Renal pelvis & ureteral tumors.

• 2ry.

BENIGN TUMORS 1. Renal cortical adenoma: o Micro-scopic: Small well differentiated glandular renal cortical tumor. • Clinical picture: Usually asymptomatic.

However, any adenoma regardless its size should be considered as early RCC. 2. Renal Onco-cytoma: o Micro-scopic: Large epithelial cells with fine granular eosino-phillic cytoplasm. o Macro-scopic: It has a well defined fibrous capsule. • Treatment: Excision. 3. Angio-myo-lipoma (hamartoma) “rare”: o Micro-scopic: 3 histological components: blood vessels, smooth muscle & fat cells. o Macro-scopic: Encapsulated, yellow grey & causes renal bulge. • Investigations: US & CT are diagnostic. • Treatment: o < 4 cm: Follow up every year (US &/or CT) o > 4 cm without complaint: Follow up every 6 months. o > 4 cm with complaint: Nephron sparing surgery.

RENAL CELL CARCINOMA (RCC) WILM'S TUMOR (NEPHRO-BLASTOMA) RENAL PELVIS & URETERAL TUMORS

INCIDENCE

• 2.5% of adulthood cancer. • 85% of 1ry renal tumors. • More common in blacks than whites.

• 10% of childhood cancer. • 80% of pediatric urologic malignancies. • 90% before the age of 7 years with a peak

at 3 years.

• 5% of all urologic malignancies. • Age: 65 years. • Male to female ratio is 2:1.

ETIOLOGY

• Occupational exposure to cadmium & asbestos.

• Cigarette smoking. • Chromosomal abnormalities. • Genetic malformations.

• Abnormal proliferation of meta-nephric blastoma.

• Occupational exposure to certain dyes & solvents.

• Cigarette smoking & excessive coffee intake. • Analgesic abuse. • Chronic irritation (stones & infections).

PATHOLOGY Origin o Proximal convoluted tubules (PCTs). o Renal or extra-renal. 1. TCC (90%):

o Usually localized at the time of diagnosis o 20% are papilloma (25% are single & 50%

are multiple). 2. SCC (10%): o Usually due to chronic irritation & sessile. o Rare in the ureter. 3. Adeno-carcinoma (very rare).

Micro-scopic

• Mixed adenoma (clear, granular or sarcomatoid cells).

1. Clear cell (75%). 2. Chromo-phobe (5%). 3. Papillary (15%).

• Adeno-myo-sarcoma with 2 histological sub types:

o Favorable. o Unfavorable.

Macro-scopic

• It has no true capsule, usually rounded & causes renal bulge.

• Cut surface is yellow orange.

• Solitary, large & well demarcated. • Cut surface is grey with areas of hemorrhage

& necrosis.

Spread • Direct to surrounding structures, renal vein & systemic circulation.

Staging • Stage I: Tumor confined to the kidney. • Stage II: Peri-nephric fat invasion but still in

the Gerota's fascia. • Stage III: o III A: Renal vein or IVC invasion. o III B: Regional LNs invasion. o III C: Regional LNs & local blood vessels

invasion. • Stage IV: o IV A: Extension to surrounding structures. o IV B: Distant metastasis.

• Stage I: Tumor confined to the kidney & completely excised.

• Stage II: Tumor extends beyond the kidney but completely excised.

• Stage III: Tumor confined to the abdomen

without hematogenous metastasis • Stage IV: Hematogenous metastasis. • Stage V: Bilateral Wilm's tumor.

• T0: No evidence of 1ry tumor. • Ta: Tumor confined to mucosa. • Tis: Carcinoma in situ (CIS). • T1: Sub-mucosal invasion. • T2: Muscular invasion. • T3: Peri-ureteral or peri-pelvic fat invasion. • T4: Extension to surrounding structures.

Grading • According to nuclear size, irregularities (dysplasia) & prominence.

• I - IV grades (grade IV is highly malignant).

CLINICAL PICTURE

1. Classic triad: Hematurea, loin pain & abdominal mass.

2. Para-neoplastic syndrome (40%):

Fever, weight loss, erythro-cytosis & hyper-calcemia.

3. Symptoms & signs of metastasis (30%). ü Diagnosis is mainly clinical.

1. Abdominal mass (75%). 2. Abdominal pain (30%). 3. Hypertension (45%). 4. Hematurea (25%) 5. Distension, anorexia, nausea & vomiting. 6. Symptoms & signs of metastasis (varicocele,

brain &/or pulmonary metastasis) “rare”.

1. Frank hematurea (70-90%). 2. Flank pain (8-50%). 3. Flank mass (10-20%). 4. Irritative voiding symptoms (10-20%). 5. Symptoms & signs of metastasis.

INVESTIGATIONS • Lab. • Hematurea, anemia & high ESR.

• Erythro-cytosis & hyper-calcemia. • Microscopic hematurea & anemia. • Disturbed liver function.

• Hematurea & pyuria. • Urine cytology depends on the grade. • Elevated liver enzymes.

• Rad. 1. US

• The best diagnostic tool for renal mass (cyst) (sensitivity 75%). • Solid mass. • Detects IVC invasion.

2. KUB • Shows tumor calcifications. 3. IVU • 75% accuracy in RCC diagnosis.

• Distorted pelvi-calyceal system (irregular spider leg deformity).

• Confirm the diagnosis: 1. Radio-lucent area. 2. Egg shell calcification. 3. Distorted pelvi-calyceal system. 4. Assess anatomy & function of the other

kidney.

• Filling defect.

4. CT • The gold standard for RCC diagnosis. • Enhanced mass with ↓ density.

• Filling defect.

• Diagnosis, staging & assessment of regional LNs & distant metastasis. 5. Renal

angio-graphy

• Limited value than CT. • Detects neo-vascularization, A-V fistulae,

renal & IVC invasion.

6. MRI • As sensitive as CT in staging. • Detects vascular invasion.

ü Advantages: o No contrast media or ionizing radiation.

7. Chest X-ray for pulmonary metastasis. • Needle biopsy.

• Endoscopy + biopsy, resection or fulgration.

DD

ü Flank mass in children: 1. Hydro-nephrosis. 2. Multi-cystic kidney. 3. Mesenteric cyst.

4. Neuro-blastoma. 5. Hepato-blastoma. 6. Renal & lympho-

sarcoma.

T REATMENT

v Localized disease (stages I - III A): • Radical nephrectomy:

It is removal of the kidney, covering fascia, adrenal, proximal half of the ureter & regional LNs.

• Postoperative recurrence rate is 2-3%. v Disseminated disease: 1. Surgery: • Radical nephrectomy to relief pain &

hemorrhage. • Removal of solitary brain &/or pulmonary

metastasis. 2. Chemo-therapy: • RCC is chemo-resistant. 3. Palliative radio-therapy: • To brain &/or pulmonary metastasis. • RCC is relatively radio-resistant. 4. Hormonal therapy (progesterone or

androgen): 0-33% response. 5. Biologic response modifiers: • Purified human leuko-cytic interferon &

interleukins.

1. Surgery: • In unilateral respectable tumors. • In bilateral tumors: o With favorable histology: § Pre-operative chemo-therapy & nephron

sparing surgery. o With unfavorable histology: § Aggressive surgery & post-operative radio

& chemo-therapy. 2. Chemo-therapy: • Post-operative vincristine & actinomycin. • Wilm's tumor is chemo-sensitive. 3. Radio-therapy: • In advanced tumor (stages III & IV). • Wilm's tumor is radio-sensitive. • Dis-advantages:

1. Growth retardation. 2. Organ toxicity.

ü Prognostic factors: • Histology of the tumor. • Stage of the tumor. • LNs involvement. • Hematogenous metastasis.

1. Surgery: • Radical nephro-ureter-ectomy with bladder

cuff. • Nephron sparing surgery in:

1. Single kidney. 2. Marginal renal function. 3. Bilateral cases. 4. Low grade tumors.

2. Chemo-therapy: • Locally after aggressive resection (BCG). • Systemically with metastasis. 3. Radio-therapy: • Of limited value.

PROGNOSIS

ü 5-year survival rate: o Stage I (90-100%). o Stage II (75-95%). o Stage III (60-70%). o Stage IV (16-30%).

o Favorable histology: 4-year s.r. = 90%. o Unfavorable histology: 2-year s.r. = 60-90%. o Bilateral Wilm's tumor: 3-year s.r. = 82%.

36


BLADDER CANCER v Incidence: o It is the 2nd most common GU tumor. v Risk factors: 1. Age: It is not common before the age of 40 with a peak at 50-70 years. 2. Sex: Male to female ratio is 3:1. 3. Race: More common in whites than blacks (4:1). 4. Chronic irritation of bladder mucosa by urinary bilharziasis, stones or long-term catheters (SCC). 5. Cigarette smoking: o It is the major cause in the developed world as it contains carcinogens as 4-amino-bi-phenyl (4-ABP)

& 2-naphthyl-amine. o Smokers have a 2-5 fold ↑ risk compared to non-smokers. 6. Occupational exposure to aniline, rubber (tires & electric cables), dyes, leather, paints &

hairdressers. 7. Drugs: Prolonged use of phenacitin or cyclo-phosphamide. 8. Pelvic radio-therapy. v Pathology:

• Micro-scopic: o 1ry tumours § Uro-thelial carcinoma (most common): 1. TCC (> 90%). 2. SCC (7-8% but 75% in areas where schistosomiasis is endemic as in Egypt). 3. Adeno-carcinoma (2%). § Non-uro-thelial carcinoma (rare):

As pheo-chromo-cytoma, melanoma, lymphoma & sarcoma. o 2ry tumours: § Mostly metastatic adeno-carcinoma from the gut, prostate, kidney or ovary.

• Spread: 1. Direct to detrusor muscle, ureteral orifices, urethra, peri-vesical fat, prostate, uterus, vagina, bowel

or pelvic walls. 2. Implantation into abdominal wounds or PC catheter tracts. 3. Lymphatic to iliac & para-aortic LNs. 4. Blood to liver, lung, adrenal gland & bone.

• Grading: 1. Grage 1: Well differentiated. 2. Grade 2: Moderately differentiated. 3. Grade 3: Poorly differentiated.

37


• Staging (TNM 1997):

Tumor LNs Metastasis Tx • 1ry tumor cannot be

assessed. Nx • Regional (iliac & para-

aortic) LNs cannot be assessed.

Mx • Distant metastasis cannot be assessed.

T0 • No evidence of 1ry

tumor. N0 • No regional LN

metastasis. M0 • No distant metastasis.

Ta • Non-invasive papillary carcinoma.

Tis • CIS. T1 • Sub-epithelial CT

invasion. N1 • Single LN < 2 cm in its

greatest dimension. M1 • Distant metastasis.

T2 • Detrusor muscle invasion:

N2 • Single LN 2-5 cm or multiple LNs < 5 cm.

T2a o Inner half (superficial muscles).

T2b o Outer half (deep muscles).

T3 • Peri-vesical fat invasion: N3 • Single or multiple LNs > 5

cm.

T3a o Micro-scopic. T3b o Macro-scopic. T4 • Extension to surrounding

structures:

T4a o Prostate, uterus, vagina or bowel.

T4b o Pelvic or abdominal walls.

• Macro-scopic: 1. TCC: • It may be: o Single or multifocal (5% have renal pelvis or ureteral TCC in association with bladder TCC). o Superficial (Ta, Tis & T1) or muscle-invasive (T2, T3 &T4). • It may be: 1. Papillary (usually) (with at least 7 transitional cell layers1 covering a fibro-vascular core) which is

usually superficial. 2. Fungating or ulcerating mass which is usually muscle-invasive. 3. Flat CIS (10%) which is poorly differentiated but confined to the epithelium (intact BM).

1 Normal transitional epithelium has 5 cell layers.

38


2. SCC: • In Egypt, 80% are induced by the ova of schistosoma haematobium preceded by squamous meta-

plasia. • The prognosis of bilharzial SCC is better than the non-bilharzial because it tends to be of a lower

grade with less common metastasis. 3. Adeno-carcinoma: • 1ry adeno-carcinoma is rare & usually solid or ulcerative. • 1/3 of it originate in the urachus (the remnant of the allantois) deep to the bladder mucosa in the

bladder dome. v Clinical picture:

• Symptoms: 1. Total painless hematuria (the most common symptom = 85%). 2. Asymptomatic micro-scopic hematuria (found on routine urine testing). 3. LUTS. 4. Supra-pubic pain (late & unusual). 5. Recurrent UTIs & pneumaturia due to malignant colo-vesical fistula. 6. Bone pain, weight loss, anorexia, confusion or anuria (renal failure due to bilateral ureteral

obstruction).

• Signs: o General examination: Pallor indicating anemia due to chronic blood loss or renal impairment. o Abdominal examination:

1. Supra-pubic mass in locally advanced disease. 2. Renal mass in advanced hydro-nephrosis.

o DRE: Indurated bladder base or bladder mass above or involving the prostate. o Bi-manual examination under anesthesia for staging of the tumor. v Investigations:

• Laboratory: o Evaluation of renal function & fitness for operation. o Urine cytology is not accurate as false -ve & +ve results are common.

• Radiological: 1. Abdomino-pelvic US: o For bladder mass. o To evaluate upper UT. 2. IVU:

39


o Irregular bladder filling defect. o To rule out upper tract involvement (5%) or obstruction. 3. Abdomino-pelvic CT: Diagnosis, staging & assessment of regional LNs & distant metastasis. 4. MRI is equivalent to CT. 5. Chest X-ray & bone scan for distant metastasis.

• Cysto-scopy & biopsy: 1. Confirm the presence of the tumor & its site, size, number & gross appearance.

CIS appears as a slightly raised velvety erythematous area. 2. Biopsy should be taken from the base of the tumor including the muscle. v Treatment:

• Superficial BC (Ta, Tis & T1): 1. Trans-Urethral Resection of Bladder Tumor (TURBT):

It is complete removal of the tumor with the underlying detrusor muscle. 2. Laser photo-coagulation: • Advantage: Less bleeding. • Dis-advantage: Lack of available tissue for histo-pathological examination. 3. Intra-vesical therapy:

Chemo-therapy or immune-therapy after the initial tumor resection due to high recurrence rate after the previous lines of treatment.

1) Intra-vesical chemo-therapy: (as mitomycin C, adriamycin & thiotepa) § It is given as a single dose within 24 hours or weekly for 6 weeks starting 2 weeks after TURBT. § It is administered via a urethral catheter & retained in the bladder for 1-2 hours.

2) Intra-vesical immune-therapy: (as BCG2) § It enhances the immune response of the bladder to get rid of the residual tumor cells. § It is given weekly for 6 weeks for G3 T1 TCC & CIS starting 2 weeks after TURBT. § It is administered via a urethral catheter in 50 ml saline & retained in the bladder for 1-2 hours.

ü Follow up after TURBT & intra-vesical therapy: o Cysto-scopy & urine cytology every 3 months for 2 years to detect any recurrence.

Then every 6 months for 3 years. Then annually thereafter.

o Radical cystectomy for rapidly recurring multi-focal tumors especially those of high grade or associated with CIS.

2 It is an attenuated strain of mycobacterium bovis used for TB vaccination.

40


• Localized muscle-invasive BC (T2 – T3a): 1. Radical cystectomy: (the standard treatment for patients fit for surgery) • It is removal of:

1. The urinary bladder with its peritoneal covering, urachal remnant & peri-vesical fat. 2. Prostate, seminal vesicles & pelvic vas deferens in males.

Uterus, fallopian tubes, ovaries & anterior vaginal wall in females. 3. Lower ureters & pelvic LNs.

2. Urinary diversion:

It is an integral part of this operation & includes:

1) Uretero-cutaneous diversion: Re-implantation of the ureters into the skin.

2) Uretero-sigmoidostomy: Re-implantation of the ureters into the sigmoid colon. Ø Complications:

Hyper-chloremic acidosis, ascending infection & malignancy at the site of anastomosis.

3) Ileal conduit: Re-implantation of the ureters into an isolated ileal segment which is connected to the skin.

4) Orthotopic ileal neo-bladder (Kock pouch & Tanta pouch):

Formation of a neo-bladder from an isolated ileal segment which is connected to the urethra & the ureters are re-implanted into it.

3. Partial cystectomy: • For very selective cases of small solitary domal tumour (especially urachal adeno-carcinoma) where

1-2 cm free margin can be obtained & a good capacity bladder is left behind. 4. Radio-therapy: • Only 30-40% of cases have complete response. Ø Complications: Radiation cystitis & proctitis. 5. External beam radiation: • 6000 rads over a period of 6 weeks.

• Locally advanced (T3b - T4) & metastatic BC: 1. Systemic chemo-therapy: • Methotrexate, Vinblastin, Adriamycin & Cis-platin (MVAC). • Only 10-15% of cases have complete response. 2. Palliative radio-therapy. 3. Salvage cystectomy: • For cases with intractable hemorrhage not responding to other lines of treatment.

41


PROSTATE CANCER v Incidence: o It is the most commonly diagnosed malignancy of males in the US. v Risk factors: 1. Age: 60-70% of males have histological evidence of occult carcinoma by the age of 80 years 2. Race: More common in blacks than whites. 3. Family history: 1st degree relatives of males with PC have 2-3 fold ↑ risk. 4. Sex hormones: o PC is often sex hormone dependent & can regress when androgen stimulation is removed. o Males castrated at an early age rarely develop PC. 5. BPH can occur in conjunction with PC. 6. Cigarette smoking. 7. Diet: High fat intake. 8. Occupational Exposure to pesticides, leather & cadmium. v Pathology:

• Micro-scopic: 1. Adeno-carcinoma (95%) from the acinar epithelium. 2. TCC & SCC (rare). ü 75% of PC arise from the peripheral zone.

• Spread: 1. Direct to seminal vesicles, peri-prostatic tissue, urethra, ureters & rectum (rare as the Denonvillier

fascia act as a natural barrier). 2. Lymphatic to obturator, iliac (internal, external & common) & para-aortic LNs. 3. Blood to:

o Bone (90%) mainly the vertebrae, neck of femur, pelvic bone & ribs. It is usually osteo-blastic but may be osteo-lytic.

o Liver & lung (late).

• Grading: (Gleason grading system) o According to the low power appearance of the glandular architecture under microscope. o It recognizes 5 growth patterns of invasive adeno-carcinoma. o Gleason scores:

1) 2-4: Well differentiated (low grade 1) adeno-carcinoma. 2) 5-7: Moderately differentiated (intermediate grade 2) adeno-carcinoma. 3) 8-10: Poorly differentiated (high grade 3) adeno-carcinoma.

42


• Staging (TNM):

Tumor LNs Metastasis Tx • 1ry tumor cannot be

assessed. Nx • Regional LNs cannot be

assessed. Mx • Distant metastasis

cannot be assessed.

T0 • No evidence of 1ry tumor.

N0 • No regional LN metastasis.

M0 • No distant metastasis.

Tis • CIS. T1a • 5% of tissue in resection

for benign disease has cancer - normal DRE.

N1 • Metastasis in 1 or more regional LNs.

M1a • Distant metastasis in non-regional LNs.

T1b • > 5% of tissue in resection for benign disease has cancer - normal DRE.

M1b • Distant metastasis to bone.

T1c • Tumor detected from ↑ PSA alone - normal DRE & TRUS.

M1c • Distant metastasis to other sites.

T2a • Tumor palpable by DRE

or visible by TRUS on one side only - confined to prostate.

T2b • Tumor palpable by DRE or visible by TRUS on both sides - confined to prostate.

T3a • Extra-capsular extension

on one or both sides.

T3b • Seminal vesicle involvement.

T4 • Extension to bladder

neck, sphincter, rectum, levator muscles or pelvic walls.

43


v Clinical picture: ü Symptoms & signs appear late in the disease. 1. Bladder Outlet Obstruction (BOO) (voiding dys-function):

o Difficult micturation or incontinence. 2. Hematuria (more common with BPH than with PC). 3. Hemato-spermia due to involvement of the seminal vesicles. 4. Priapism due to involvement of the corporeal bodies. 5. Abdominal mass & constipation. 6. Ureteral obstruction in advanced disease. 7. DRE:

1. Hard nodule or irregular induration in a part or the whole of the gland. 2. Obliteration of the median sulcus.

ü Normal DRE does not exclude PC. v Investigations:

• Laboratory: 1. ↑ prostatic acid phosphatase in 75% of patients with extra-capsular or distant metastasis. 2. ↑ Alkaline phosphatase in bone or hepatic metastasis. 3. Prostatic specific antigen (PSA): • It is very important in diagnosis (tumor specific) & follow-up. • Normal value: 0-4 ng/ml. • It may be ↑ in non-malignant conditions as prostatitis or prostatic infarction. • Types:

Free & combined. Free to combined ratio is 1:4.

• Forms:

1) Age adjusted PSA: § 40-49 years: < 2.5 ng/ml. § 50-59 years: < 3.5 ng/ml. § 60-69 years: < 4.5 ng/ml. § > 70 years: > 4.5 ng/ml.

2) PSA velocity: It is PSA change over a certain period of time. § Values ≥ 0.75 ng/ml/year is suggestive of PC.

3) PSA density: It is the total PSA (ng/mL) divided by prostatic volume (cm3) as estimated by TRUS. § The cut-off is 0.15 ng/ml.

44


4) Free/Total PSA < 20%: Mostly cancer prostate. 4. Blood analysis & renal function tests.

• Radiological: 1. Abdominal US to evaluate upper UT. 2. TRUS: o Hypo-echoic appearance due to ↓ acinar/stromal ratio. o The higher the grade the more hypo-echoic (progressive loss of glandular elements). 3. CT: Diagnosis, staging & assessment of regional LNs & distant metastasis. o It is done if PSA is > 20 ng/ml. 4. MRI: o For extra-capsular extension:

1. Irregular capsular bulge. 2. Obliteration of the recto-prostatic angle. 3. Asymmetry of the N-V bundles.

5. X-ray of the chest, pelvis & spine for distant metastasis 6. Bone scan by Technetium 99 for areas of ↑ bone activity (hot spots).

• TRUS guided biopsy: o It is done if abnormal DRE &/or ↑ PSA. o Biopsy from hyper-echoic lesions + 6 areas from the prostate. v Treatment:

• Localized PC (T1 - T2b) N0M0: 1. Watchful Waiting: (deferred treatment & active monitoring) • It is to postpone treatment until tumor activity occurs (rising PSA or deteriorating histo-pathological

factors on repeated biopsy). 2. Radical prostatectomy: • It is removal of the prostate, seminal vesicles & distal ends of the vas differences. • The bladder is then anastomosed to the membranous urethra. • Routes:

o Open: § Retro-pubic. § Perineal.

o Laparoscopic: • Retro-peritoneal. • Trans-peritoneal.

o Robotic.

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3. Radio-therapy: • Usually done for patients unfit for surgery. • Types:

o 3 D Radiation therapy (3DRT): 70 Gy over 5 weeks. o Brachy-therapy: TRUS guided implantation of radio-active material into the prostate.

4. Cryo-therapy: It is destruction of PC by freezing.

• Locally advanced PC (T2c - T3) N0M0: 1. Watchful Waiting: • Usually done for patients unfit for surgery. 2. Radical prostatectomy: • After neo-adjuvant hormonal therapy (NHT) to ↓ prostate size & PSA. 3. Radio-therapy & Hormonal therapy: • Forms of hormonal therapy:

o Neo-adjuvant (before radio-therapy). o Concomitant & adjuvant (during & after radio-therapy). o Adjuvant (after radio-therapy).

• Types of hormonal therapy:

o Surgical castration. o Medical castration: § Estrogen. § LHRH agonists as Goserelin acetate & Leuprolide acetate. § Steroidal anti-androgens as medroxy-progesterone acetate. § Pure anti-androgen as Bicalutamide, flutamide & nilutamide.

4. Chemo-therapy: • Usually given for patients with hormonal resistant PC.

• Metastatic PC: 1. Hormonal therapy. 2. Chemo-therapy.

46


TESTICULAR TUMORS v Incidence: • 2 % of all male cancer. • Bi-modal age distribution:

o 1st peak (pre-pubertal): 2 - 4 years. o 2nd peak: 25 - 35 years (most common malignancy before the age of 50 years).

v Etiology & predisposing factors: 1. UDT. 2. Gondal dys-genesis, androgen in-sensitivity & inter-sex. 3. +ve family history (2%). v Pathology:

• Classification: o 1ry: 1. Germ Cell Tumors (GCT):

• Seminoma: § Most common adult testicular tumor (extremely rare pre-pubertal). § Sub-types: Classic, spermatocytic & anaplastic.

• Non-seminoma: § Yolk sac tumor: Most common pre-pubertal testicular tumor. § Teratoma: Consists of all 3 embryonic layers. § Embryonal carcinoma: Most un-differentiated testicular tumor. § Chorio-carcinoma.

2. Sex cord (stromal) tumors. 3. Mixed (gonado-blastoma). o 2ry: • Leukemia (more in children & commonly bilateral). • Lymphoma (more in elderly).

• Spread: o Lymphatic to para-aortic & para-caval retro-peritoneal LNs, mainly at the level of the renal hilum

(2nd lumbar vertebra “L2”). Cross of lymphatics may occur from the right to the left side but not the reverse.

o Blood (advanced tumor) to lung, liver, brain, bone, kidney & adrenals.

• Staging: 1. Stage I: Tumor confined to the testicles. 2. Stage II: Retro-peritoneal LNs involvement. 3. Stage III: Distant metastasis.

47


• Staging workup: o Evaluation of regional retro-peritoneal LNs by abdominal CT or MRI. o Evaluation of distant metastasis by: § Chest X-ray. § Tumor markers measurement few days after orchiectomy.

v Clinical picture: 1. Heterogenous consistency or stony hard irregular mass. 2. No pain nor tenderness. 3. Absent testicular sensation. 4. Symptoms & signs of metastasis. v Investigations:

• Radiological: o Scrotal US: Detects testicular tumor & determines its texture (solid or cystic).

• Laboratory: o Tumor markers: § Beta-subunit of HCG, α-feto-protein & lactic de-hydrogenase. ü normal markers do not exclude testicular tumor. o Blood analysis: § Anemia in patients with disseminated metastasis. v Treatment: • Radical orchiectomy through inguinal approach with ligation of spermatic cord at the internal ring. • Adjuvant therapy: o Seminoma GCT:

1. Radio-therapy on the pelvis & LNs (radio-sensitive). 2. Retro-peritoneal LNs dissection. 3. Chemo-therapy.

o Non seminoma GCT:

1. Retro-peritoneal LNs dissection. 2. Chemo-therapy.

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DIFFERENTIAL DIAGNOSIS

v Differential diagnosis of scrotal swellings: o Skin: 1. Lymphodema & elephantiasis. 2. Sebaceous cyst. 3. Epithelioma. o Tunica: • Vaginal hydro-cele, hemato-cele, pyo-cele & chylo-cele. o Testis: 1. Trauma (intra-testicular hematoma). 2. Torsion. 3. Tumor “see classification in page 44”. 4. Inflammation (orchitis):

• Acute: bacterial & viral (mumps). • Chronic: non-specific epididymo-orchitis & syphilitic gumma.

o Epididymis: • Epididymitis (acute & chronic). o Urethra: 1. Peri-urethral abscess. 2. Trauma to bulbar urethra with urine extravasation.

v Differential diagnosis of inguino-scrotal swellings: 1. Complete oblique inguinal hernia. 2. UDT at scrotal neck. 3. Structures in the spermatic cord:

• Hydro-cele (congenital, infantile & encysted). • Varico-cele (1ry & 2ry) & lympho-cele. • Lipoma. • Funiculitis (inflammation of the spermatic cord).

v Differential diagnosis of inguinal swellings: 1. Reducible swellings:

• Inguinal hernia: direct & oblique. • Femoral hernia. • Saphena varix.

2. Cystic swellings: Cold abscess & psoas bursitis. 3. Solid swellings: Inguinal LNs & UDT. 4. Pulsating swellings: Ilio-femoral aneurysm & A-V fistula.

49


OBSTRUCTIVE UROPATHY

v Prune belly syndrome: From Wikipedia, the free encyclopedia, in short with some modifications.

• Background: o It is a congenital disorder of the urinary system affecting about 1/40.000 births (about 97% are

males). • Synonyms: o Abdominal Muscle Deficiency Syndrome, Congenital Absence of the Abdominal Muscles, Eagle-

Barrett Syndrome, Obrinsky Syndrome, Fröhlich Syndrome, or rarely Triad Syndrome. • Symptoms 1. A partial or complete lack of abdominal muscles.

There may be wrinkly folds of skin covering the abdomen (hence its name). 2. UDT in males. 3. UT abnormality such as unusually large ureters, distended bladder & VUR. 4. UTIs.

50


OBSTRUCTIVE UROPATHY v Definition: o UT dilatation due to obstruction. v Patho-physiology: o Kidneys receive about 25% of resting CO (About 1 L of blood). o Renal plasma flow is about 600 ml/min which yields a GFR of about 120 ml/min. o The renal tubules re-absorb 99% of the filtrate leaving a final urine output of 1-1.5 L/day. § In a normally functioning kidney, urine formed within the tubular system empties into the calyces,

where pacemaker sites generate peristalsis to propel urine into the pelvis. § Urine is conveyed into the ureter, where further peristalsis moves it in boluses into the bladder. o The collecting system has a baseline pressure of 0-10 cm water. o This pressure ↑ with peristalsis up to 20-60 cm water & with obstruction (especially acute

conditions) up to 80 cm water. § Obstruction → ↑ ureteral & renal pressure→ hydro-nephrosis → ↓ RBF & GFR → obstructive

nephropathy → renal failure. v Causes of obstructive nephropathy:

KIDNEYS URETERS BLADDER,PROSTATE & URETHRA

CONGENITAL

• Poly-cystic kidney. • Renal cyst. • PUJ obstruction.

• Valve. • Stricture. • Uretero-cele. • UVR. • Retro-caval ureter. • Prune belly syndrome.

• Posterior urethral valve. • Urethral stricture. • Hypo-spadias. • Epi-spadias. • Phimosis. • Hydro-colpos

NEOPLASTIC • RCC. • Willm’s tumor. • TCC of the renal pelvis.

• Carcinoma (1ry or metastatic).

• Bladder, prostatic, penile or urethral carcinoma.

INFLAMMATORY

• Tuberculosis. • Echino-coccus

granulosus.

• Tuberculosis. • Schistosomiasis. • Abscess. • Ureteritis cystica.

• Para-urethral abscess.

METABOLIC • Stones.

MISCELLANEOUS

• Renal artery aneurysm. • Trauma. • Sloughed papillae.

• Aortic aneurysm. • Trauma. • Retro-peritoneal fibrosis. • Radio-therapy. • Lympho-cele. • Urinoma. • Pregnancy. • Endometriosis.

• BPH. • Neuro-genic bladder.

51


v Clinical picture: o Acute obstruction: § Uni-lateral: Renal colic & renal pain. § Bi-lateral: Anuria.

o Chronic obstruction:

1. Asymptomatic. 2. Hydro-nephrosis. 3. Renal failure (uremia) in bilateral obstruction. 4. Hypertension, hyperkalemia 2ry to RTA & salt wasting predisposing to extra-cellular fluid volume

depletion. v Investigations:

• Laboratory: o Urine analysis: Hematuria, necroturia, crystaluria, casts & proteinuria. o Renal function tests:

1. Blood urea: normal 20-40 mg%. 2. Serum creatinine: normal < 1.2 mg%. 3. Creatinine clearance: normal 80-120 ml/min.

• Radiological: 1. US differentiates solid from cystic swelling. 2. KUB detects radio-obaque shadows. 3. IVP detects renal function & cause of obstruction. 4. MRI detects cause of obstruction in non functioning kidney. 5. CT for diagnosis of tumors, staging & assessment of regional LNs & distant metastasis.

• Radio-isotope study: detects: 1. Split renal function. 2. GFR. 3. Degree of obstruction (Diuretic isotope scan).

• Uro-dynamic studies. v Treatment: 1. Treatment of the cause as stone, stricture, … 2. Corrective surgery as UPJ obstruction, uretero-cele, … 3. Palliative diversion if the cause of obstruction is irremovable as:

• Cystostomy in urethral stricture. • PCN in hydro-nephrosis.

4. Nephrectomy if non-functioning kidney.

52


URINARY STONES v Definition: They are abnormal concretions occurring anywhere along the collecting system of the

UT & consist of crystalline components incorporated in an organic matrix. v Incidence: o It is one of the most common diseases of the UT. o Male to female ratio is 3:1. o Age: 30-50 years. v Etiology & pathogenesis: “multi-factorial process”

• Factors influencing stone formation: 1. Genetic (enzymatic disorders) as in cystinuria & RTA. 2. Environmental as in hot climate with ↓ fluid intake & disturbed diet.

• Theories of stone formation: 1. Super-saturation: Spontaneous nucleation of crystals begins when high saturation is reached. 2. Nidus: Precipitation of crystals over a FB (blood clot or pus). 3. Absence or low concentration of urinary Inhibitors which are substances that block crystallization

e.g. pyro-phosphate, citrate, magnesium, zinc & macro-molecules. v Types Calcareous (Ca) stones (75%) Non-calcareous stones (25%) Ca phosphate Ca oxalate Struvite3 (15-

20%) Cystine (4-8%) Uric acid (1-2%)

• Et

iolo

gic

fact

ors

of s

peci

fic

ston

e ty

pes

1. Urinary super-saturation with Ca due to:

o Absorptive hyper-calciuria due to ↑ intestinal absorption of Ca.

o Renal hyper-calciuria due to impaired tubular absorption of Ca.

o Resorptive hyper-calciuria due to hyper-para-thyroidism.

2. Hyper-oxaluria due to ↑ intestinal absorption of oxalate 2ry to fat mal-absorption or intestinal by-pass (Ca oxalate stone).

o Infections with bacteria having urease activity which splits urea into ammonia rising the pH & thus ↓ the solubility of magnesium ammonium phosphate.

o Cystinuria which is an inherited renal tubular absorption defect of cystine, ornithine, lysine & arginine (COLA).

o Low urinary pH.

o Low urinary volume.

o Hyper-uricosuria.

Degree of radio-opacity

o Very Radio-opaque.

o Radio-opaque.

o Moderately … o Slightly … o Non-opaque

o (++++) o (+++) o (++) o (+) o Radio-lucent.

Color o Yellow. o Brown. o Yellow. o Whitish. o Reddish

brown. Charact

ers o Tend to be

stag-horn. o Small &

multiple. o Tend to be

stag-horn. o Small & multiple.

3 Magnesium ammonium phosphate.

53


RENAL STONES • Any type of the above mentioned stones can occur in the pelvis, calyces or pelvi-calyceal system. v Clinical Picture: o Symptoms: ü Small stones are more symptomatic than large ones. 1. Asymptomatic (silent & discovered accidently): § If the stone is small & trapped in a minor calyx. § Also, stag-horn stones may be asymptomatic.

2. Renal colic (intermittent obstruction or movement of stones). 3. Renal pain. 4. GIT symptoms: Nausea, vomiting & abdominal distention (paralytic ileus with acute renal colic). 5. Haematuria (gross or microscopic). 6. Fever & chills (if there is infection). o Signs: 1. Tenderness in the costo-vertebral (renal) angle & muscle rigidity over the kidney may be present. 2. The abdomen is distended, tympanitic & quiet on auscultation. 3. Loin mass may be seen, felt or percussed (marked hydro-nephrosis due to prolonged obstruction). v Investigations:

• Laboratory: o Urine analysis:

1. Hematuria (gross or microscopic). 2. Pyuria (if there is infection). 3. Crystals. 4. Urinary pH: § If alkaline, the stone is struvite. § If acidic, the stone may be cystine or uric acid.

o Blood analysis:

1. Leuco-cytosis (if there is infection). 2. High blood urea & serum creatinine (If renal function is not adequate). 3. High Serum uric acid in patients with uric acid stone formers.

• Radiological: 1. KUB detects the site & size of radio-paque stones. 2. IVU detects: o Serum creatinine before doing it. o The site of obstruction. o Non-opaque stones as filling defects.

54


3. US: o Differentiates non-opaque stones from other filling defects on IVU. o Detects hydro-nephrosis, associated renal masses or parenchymal atrophy. 4. Retro-grade uro-graphy (rarely needed). 5. CT: o Differentiates non-opaque stones from tumors or blood clots. o Non contrast CT is helpful in patients with compromised renal function. 6. Radio-nuclide reno-graphy: o Determines renal function in a poorly functioning kidney before surgical intervention. v Complications: 1. Hematuria leading to anemia. 2. Obstruction leading to hydro-nephrosis, hydro-calycosis & renal failure. 3. Infection: phyelo-nephritis & pyo-nephrosis. 4. Migration to the ureter or urinary bladder. 5. Malignancy in long standing stones (chronic irritation) with infection & metaplasia. v Treatment:

• Medical: Ø Indications: Single, smooth & small stone (< 1/2 cm) with patent UT. Ø Methods: “3Ds” 1. Dilution (maintenance of large urine volume by ↑ fluid intake). 2. Drugs:

o Ortho-phosphates ↓ urinary Ca. o Hydro-chlor-thiazide prevents re-absorption of Na & Ca in the loop of Henle & thus ↓ total

urinary Ca excretion.

o Potassium or magnesium citrate ↑ urinary inhibitors.

o Allopurinol is used in uric acid stones. o Urinary alkalinization with 1/6 molar Na lactate or Na or K bi-carbonate to dissolve uric acid

stones. 3. Diet regulation:

o Limited sodium & oxalate. o Limited dairy products in patients with absorptive hyper-calciuria. o Limited animal proteins in patients with gout & hyper-uricosuria.

55


• Surgical: 1. Extra-corporeal Shock Wave Lithotripsv (ESWL): o A focused high-pressure shock wave to fragment the stone. o It is best for renal stones < 2.5 cm.

Contra-indications: o Pregnancy, morbid obesity, bleeding diathesis, large or stag-horn stones & distal obstruction. 2. Per-Cutaneous Nephrosto-Lithotomy (PCNL): o A nephrostomy tube is placed in the kidney after a flank puncture. o The stone is manipulated & removed by the nephro-scope. o Stones may be fragmented by ultra-sonic or laser probes. o It is indicated for large (> 2.5 cm) or stag-horn stones. 3. Combined ESWL & PCNL: o Large or stag-horn stones often require initial debulking with PCNL followed by ESWL for residual

stones. 4. Open surgical treatment:

1) Pyelo-lithotomy: Removal of the stone through the renal pelvis after a flank incision. 2) Nephro-lithotomy: Removal of the stone through renal parenchymal incision. 3) Anatrophic nephro-lithotomy: Removal of a stag-horn stone through a longitudinal incision on

the convex surface of the kidney.

4) Partial nephrectomy for recurrent stones in the lower calyx. 5) Nephrectomy for renal stones with loss of renal function. 6) Nephrostomy when the general condition of the patient prevents definite treatment.

56


URETERAL STONES • They originate in the kidney & spontaneously pass into & down the ureter by gravity & peristalsis. • The stone is arrested in the narrowest points of the ureter:

1. At the UPJ. 2. Where the ureter crosses over the iliac vessels. 3. At the UVJ.

v Clinical Picture: o Symptoms: 1. Renal colic. 2. Renal pain. 3. Renal mass (if obstructed ureter). 4, 5 & 6 (as in renal stones). o Signs: 1. Marked tenderness in the costo-vertebral (renal) angle & flank. 2. The abdomen is distended, tympanitic, & quiet on auscultation. 3. Hyper-sensitive & retracted ipsilateral testis if the stone is in the upper ureter. 4. Hyper-esthetic scrotal skin if the stone is in the lower ureter. v Investigations: • As in renal stones. v Treatment:

• Medical: As in renal stones + o Stone expulsive therapy for stones in the lower ureter < 0.8 cm (80% success rate):

1. Ca channel blockers. 2. α-blockers. 3. Cortico-steroids.

• Surgical: 1. ESWL is best for stones in the upper ureter especially with ureteral stenting. 2. Uretero-scopy:

o Small stones may be grasped directly or engaged in a stone basket & extracted. o Large stones may be fragmented by electro-hydraulic, pneumatic, ultra-sonic or laser lithotripsy.

3. Uretero-lithotomy if other methods fail.

57


BLADDER STONES • They are caused by bladder outlet obstruction (BOO) or FBs (portions of catheters or sutures). • More common in males. v Clinical Picture: • Urgency, frequency & interrupted stream. v Investigations:

• Laboratory: • Urine analysis: o Pyuria & hematuria.

• Radiological: 1. KUB detects radio-paque stones. 2. US detects radio-lucent stones. 3. IVU detcts:

o Back pressure changes in the kidneys. o Residual urine volume.

v Treatment: 1. Litho-trites: o They are mechanical devices that permit crushing of large & hard bladder stones under direct vision. o The fragments are then washed out through a cysto-scopic sheath. 2. Electro-hydraulic or ultra-sonic lithotripsy. 3. Cysto-lithotomy through a small supra-pubic incision.

PROSTATIC STONES • It is a rare condition affecting old males. • It is due to calcification of the corpora amylaecea associated with BPH.

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BENIGN PROSTATIC HYPER-PLASIA (BPH) • It is a non-cancerous enlargement of the prostate that may restrict urinary flow from the bladder. v Incidence: o It affects about 1/3 of males older than 50 years. o About 90% of males have histological evidence of BPH by the age of 80 years. v Zonal anatomy of the prostate & patho-physiology: o The prostate is walnut-sized & forms a part of the male reproductive system. o It is composed of several regions or lobes enclosed by a capsule. o It is composed of 3 zones: central, transition & peripheral + anterior fibro-muscular stroma. o BPH arises from the transition zone while PC arises from the peripheral zone. o The transition zone which surrounds the urethra enlarges with age in a hormonally dependent

manner. o Castrated males do not develop BPH. o Enlarged prostate → infra-vesical obstruction → obstructive & irritative LUTS → bladder

hypertrophy & diverticulae formation. v Clinical picture: • Symptoms:

Obstructive Irritative General 1. Hesitancy. 2. Weak stream & straining. 3. ↓ caliber of stream. 4. Post-micturation drippling. 5. In-complete evacuation of the bladder.

1. Urgency. 2. Frequency. 3. Nocturia.

1. Anemia. 2. Renal insufficiency. 3. Renal failure (10%).

• Signs: DRE detects: 1. Size of the prostate. 2. Depth of lateral sulci (recess between prostate & lateral rectal wall). 3. Abnormal consistency (hard nodule). v Differential diagnosis: 1. Neuro-genic bladder. 2. Bladder CIS. 3. Urethral stricture from trauma or STD. 4. Cystitis & prostatitis. v Investigations:

• Laboratory: 1. Urine analysis: Hematuria. 2. PSA: Normal.

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• Radiological: 1. Abdominal or TR US:

o Detects size of the prostate & residual urine volume. o To evaluate upper UT.

2. KUB to rule out stones. 3. IVP if suspicious upper UT abnormalities.

• International Prostate Symptom Score (IPSS): § It is a set of 7 questions that yield reproducible & quantifiable information regarding symptoms &

response to treatment. § Each question allows the patient to choose 1 of 6 answers indicating increasing severity of

symptoms on a scale of 0-5.

In the past month Not at

all < 1 in 5 times

< ½ the time

About ½ the time

> ½ the time

Almost always

Your score

• Incomplete emptying: How often have you had the sensation of not emptying your bladder?

0 1 2 3 4 5

• Frequency: How often have you had to urinate < every 2 hours?

0 1 2 3 4 5

• Inter-mittency: How often have you found you stopped & started again several times when you urinate?

0 1 2 3 4 5

• Urgency: How often have you found it difficult to post-pone urination?

0 1 2 3 4 5

• Weak stream: How often have you had a weak urinary stream?

0 1 2 3 4 5

• Straining: How often have you had to strain to start urination?

0 1 2 3 4 5

None 1 time 2 times 3 times 4 times 5 times • Nocturia:

How many times did you typically get up at night to urinate?

0 1 2 3 4 5

Total I-PSS score

Score 1-7: mild 8-19: moderate 20-35: severe

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• Optional tests: 1. Uro-flow-metry: § It is useful in initial assessment & to determine the response to treatment. § A Q max value > 15 ml/s is considered normal while a value < 7 ml/s is considered low. 2. Residual urine volume: § It can be detected invasively by catheter but is best detected non-invasively by US. 3. Pressure flow (uro-dynamic) studies: § Differentiates poor bladder contraction ability (detrusor under-activity) from bladder outlet

obstruction (BOO). § BOO is characterized by high intra-vesical voiding pressure (> 60 cm water) accompanied by low

urinary flow rate (Q max < 15 ml/s). 4. Endoscopy of the lower UT for patients in whom an invasive treatment is scheduled. v Complications of BOO 2ry to BPH: 1. Gross hematuria. 2. Urinary retention. 3. Bladder stones. 4. Recurrent UTIs. 5. Renal failure (uremia) “rare”. v Treatment:

• Medical: 1. α-adrenergic blockers:

Action: ↓ resistance along the bladder neck, prostate & urethra by relaxing the smooth muscle & thus improving urinary flow.

Examples: § Non-selective α-blockers as phenoxy-benzamine. § Selective short-acting α-1 blockers as pra-zosin & alfu-zosin. § Selective long-acting α-1 blockers as doxa-zosin. § Selective α-1a blockers as tamsulosin.

2. 5 α-reductase inhibitors:

Action: block androgen action in tissues whose function is dependent on continuing production of DHT, including prostate & hair follicles. Examples: § Finasteride (Proscar) “4-aza-steroid” selectively blocks type II 5 α-reductase → inhibition of DHT-

receptor complex formation → profound ↓ in the concentration of DHT in plasma → consistent ↓ in prostate size.

§ It improves urinary flow & symptoms in 1/3 of patients.

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3. Phyto-therapeutic agents:

They are used in the treatment of LUTS 2ry to BPH. They are extracted from the roots, seeds, bark or fruits of plants.

Actions:

1. Anti-androgenic. 2. Anti-estrogenic. 3. 5 α-reductase inhibition. 4. α-receptor blockage. 5. Anti-edematous. 6. Anti-inflammatory. 7. Prostatic cell proliferation inhibition. 8. Interference with prostaglandin metabolism. 9. Protection & strengthening of detrusor muscle.

• Surgical: Ø Indications: 1. Failed medical treatment. 2. Gross hematuria. 3. Resistant urinary retention. 4. Impending renal insufficiency. Ø Methods: 1. Open prostatectomy:

Routes: 1. Supra-pubic. 2. Retro-pubic. 3. Perineal.

Indications: 1. Very large prostate (> 75 g). 2. Concomitant bladder stones or diverticulae. 3. Patients who cannot be positioned for trans-urethral surgery.

Procedure: 1. Hospitalization, general/regional anesthesia & lower abdominal incision. 2. The inner core of the prostate (adenoma) which represents the transition zone is shelled out leaving

the peripheral zone. § It may result in significant blood loss requiring transfusion. § It usually has an excellent outcome in improvement of urinary flow & symptoms.

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2. Trans-Urethral Resection of the Prostate (TURP): § It has a significant risk of morbidity (18 %) & mortality (0.23 %). 3. Transurethral incision of the prostate (TUIP): § It is an alternative to TURP for small prostate. 4. Minimally invasive treatment: § High intensity focused US (HIFU). § Laser therapy. § Thermo-therapy & hyper-thermia. § Trans-urethral electro-vaporization. § Trans-urethral needle ablation (TUNA). § Intra-urethral stents. § Balloon dilation of the prostate.

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URINARY INCONTINENCE

فضائل اجلهاد واالستشهاد يف سبيل اهللامن نة أبي عادقت نول عسر الله )لمسو هليع لى اللهص( هأن قام يهمف فذكر مأن له ادي الجهبيل فس ان اللهالإميو ل باللهأفض

صلى الله ( الله رسول له فقال ؟خطاياي عني تكفر الله سبيل في قتلت إن أرأيت ،الله رسول يا :فقال رجل فقام ،الأعماللمسو هليع(: ))معإن ،ن لتي قتبيل فس الله تأنو ابرص سبتحقبل ،مم ربر غيدم((، ول قال ثمسر الله ) هليع لى اللهص

لمسو(: ))فكي ؟قلت((، قال: تأيإن أر لتي قتبيل فس الله كفري أتنع ايطايول فقال ؟خسر الله )لمسو هليع لى اللهص(: ))معن، تأنو ابرص سبتحقبل ،مم ربر غيدإلا ،م نيريل فإن الدجب هليلام عي قال السل كذل.((

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URINARY INCONTINENCE v Definition: o Involuntary leakage of urine. v Classification: 1. Stress urinary incontinence: Leakage of urine on effort, exertion, sneezing or coughing. 2. Urge urinary incontinence: Leakage of urine accompanied or immediately preceded by urgency. 3. Mixed urinary incontinence: Leakage of urine on effort, exertion, sneezing or coughing & also

accompanied or immediately preceded by urgency. 4. Overflow incontinence: Leakage of urine accompanied by retention.

It is detected clinically by incontinence accompanied by high post-void residual. 5. Continuous incontinence: Continuous leakage of urine. 6. Nocturnal enuresis: Leakage of urine during sleep only. v Differential diagnosis: • Non-urinary wetness: o Leakage of body fluids other than urine. o It can be differentiated by very high level of creatinine in urine but not in other fluids. • Non-urethral urinary incontinence: o Leakage of urine via a route other than the urethra. 1. Fistula: Vesico-vaginal , uretro-vaginal or urethra-vaginal. 2. Ureteral ectopia: § It is a congenital insertion of the ureter into an abnormal location. § If distal to the external urethral sphincter it may cause continuous incontinence (only in females). v Physiology of urinary continence: ü It requires that: 1. The urethral sphincters are competent. 2. The neurological mechanisms coordinating storage & emptying are intact. 3. The bladder neck must be:

o Closed all the time except during voiding. o Able to withstand momentary ↑ in intra-abdominal pressure.

4. Bladder: o Visco-elastic properties (compliance):

The bladder is able expand during filling with little ↑ in intra-vesical pressure. o Detrusor muscle is relaxed due to inhibition of its para-sympathetic nerves.

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5. Outlet: o The anatomic support, innervation & intrinsic tone of the bladder neck & urethra. o The 1ry continence mechanism is: § The prostatic & membranous portions of the urethra in the male. § The entire urethra in the female.

v Assessment:

• History: 1. Identification of the type of incontinence. 2. Duration of symptoms. 3. Severity described by the number of pads used or micturition diary. 4. Drugs: can cause or worsen incontinence: o Sympatho-lytics (e.g. clonidine & terazosin) can weaken sphincter tone. o Sympatho-mimetics (e.g. pseudo-ephedrine & imipramine) can cause overflow incontinence. 5. Surgical history: o Pelvic surgery (e.g. abdomino-perineal resection). o Anti-incontinence, prostate or bladder surgery. 6. Obstetric & gynecologic history: o Gravity, parity, outcome & complications. o Vaginal delivery & cesarean section. o Hysterectomy & prolonged 2nd stage. o Sexual activity. o Pain or leakage with intercourse. o Menopause & hypo-estrogenic state. 7. Neurological history: o Spinal cord surgery or injuries. o Cerebro-vascular accident. o Parkinson's disease. 8. Gastro-intestinal history o Diarrhea or constipation. o Fecal incontinence (suspicious of neurological disease). 9. Associated: o LUTS. o Pelvic organ prolapse (any introital bulge or mass).

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• Physical examination: 1. Abdominal examination may reveal: o Tenderness, masses & supra-pubic fullness (distended bladder). o Hernias & surgical scars. 2. Pelvic examination: o External genitalia may reveal: § Signs of chronic wetness (erythema & skin breakdown). § Atrophy (pale & shiny mucosa). § Labial adhesions.

o Urethral examination may reveal: § Tenderness, masses or stenosis. § Stress incontinence is exhibited on coughing or Valsalva maneuver.

o Vaginal examination may reveal: § Atrophic vaginitis or discharge. § Bimanual examination may reveal vaginal narrowing or scars (e.g. episiotomy or surgery). § Examination of the anterior & posterior vaginal walls at rest & during Valsalva maneuver may

reveal pelvic organ prolapse. § Cysto-cele: herniation of the bladder into the anterior vaginal wall. § Entero-cele: herniation of the small bowel or omentum into the vagina. § Recto-cele: herniation of the rectum into the vagina.

3. Neurological examination: o Sensory examination to locate the level of sensory deficit. § T 5 = nipple level. § T 10 = umbilicus. § L 3 = knee. § S 3-5 = perineum & labia.

o Reflexes: o Deep tendon reflexes (altered in muscular/peripheral nerve pathology). § L 3-4 = quadriceps. § L 5 - S 2 = Achilles tendon.

o Cutaneous reflexes: § T 6 - L 2 = abdominal reflex. § L 1 - 2 = cremasteric reflex

§ S 2 - 4 = bulbo-cavernosus (sacral) reflex: ü During DRE, the glans penis or clitoris is squeezed → reflex contraction of the anal sphincter &

bulbo-cavernosus muscle. ü Its absence is a reliable indicator of neurological disease. § S 2 - 5 = anal reflex.

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• Uro-dynamic studies: ü They assess lower UT function by measuring physiologic parameters (pressure, volume, flow, leak &

bladder descent). ü They help to determine the underlying patho-physiologic process & aid in making treatment

decisions. ü Components: 1. Uro-flow-metry: It is a recording of the urinary flow rate (ml/second). 2. Cysto-metro-gram: o It is a recording of the pressure volume relation-ship while filling the bladder. o It detects abnormal bladder sensation, compliance & detrusor over-activity. 3. Voiding pressure: o It is a recording of the urinary flow rate concurrently with the intra-vesical pressure. 4. Assessment of urethral function: o The detrusor leak point pressure measures the lowest intra-vesical pressure that causes leakage of

urine in the absence of detrusor contraction. o The Valsalva or abdominal leak point pressure measures the intra-abdominal pressure that causes

leakage of urine in the absence of detrusor contraction. o The urethral pressure profile:

It is a recording of the resistance at various points along the urethra. It is measured by withdrawing a perforated urethral catheter & graphing the pressure at recorded catheter lengths.

5. Electro-myo-gram: o It is a recording of the sphincter activity concurrently with the rest of exam. o Either electrodes are attached to the perineal skin or needles are placed directly into the urethral

sphincter. 6. Video-uro-dynamics: o It combines cystography with urodynamics to observe for leak point pressures & bladder descent.

• Radiological: o VCUG: § The patient is asked to strain with a full bladder & if leakage is present, it is recorded radio-

graphically § it detects the degree of cysto-cele by measuring the extent of bladder descent below the inferior

border of symphysis pubis: o 0-2 cm corresponds to grade 1 cysto-cele. o 2-5 cm corresponds to grade 2. o > 5 cm corresponds to grade 3.

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o MRI: § It detects pelvic organ prolapse. § Advantage:

It provides detailed anatomic information on the pelvic organs without radiation exposure. § Disadvantage:

It must be done in the supine position & may underestimate the degree of prolapse. v Treatment:

• Conservative: 1. Behavioral modification: o It is an education-based program that teaches patients to modify habits such as excessive fluid or

caffeine intake & delayed voiding. 2. Pelvic floor (Kegel) exercises: o By contracting the external sphincter intermittently. 3. Urethral meatal devices & inserts for women. 4. Pessary for reduction & support of pelvic organ prolapse. 5. Indwelling catheters in the form of urethral catheter or supra-pubic tube.

• Medical: o Stress incontinence: 1. α-adrenergic agonists ↑ internal sphincter tone (e.g. Pseudo-ephedrine). 2. Estrogens for post-menopausal women orally or vaginally. o Detrusor over-activity: • Anti-muscarinic agents to suppress detrusor overactivity. § Oxybutynin chloride (Ditropan) 1-4 tablets spaced out during the day (tablet = 5mg). § Tolterodine tartrate (Detrol) “competitive muscarinic receptor antagonist” 2 mg PO twice daily. § Imipramine “tricyclic anti-depressant” 10-25 mg PO qid, it closes the bladder neck & relaxes the

detrusor.

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• Surgical: o Stress incontinence:

Aims to ↑ outlet resistance to intra-abdominal pressure. 1. Urethral bulking: o Aims to ↑ outlet resistance & improve urethral coaptation e.g. Collagen, teflon, silicone or

autologous fat. 2. Retro-pubic suspension (colpo-suspension): o Aims to restore & support the bladder neck to its retro-pubic location. 3. Trans-vaginal bladder neck suspension. 4. Pubo-vaginal sling: o They are tapes placed below the bladder neck to support the urethra to supra-pubic rectus muscle. § Autologous sling materials include rectus fascia & fascia lata.

§ Allo-graft sling materials are taken from a human donor. § Xeno-graft sling materials are taken from a non-human donor & include porcine dermal &

intestinal sub-mucosal grafts. § Synthetic sling materials include: ü Mono-filament poly-propylene mesh. ü Multi-filament poly-ester mesh e.g. tension-free trans-vaginal tape (TVT).

5. Artificial urinary sphincter: o It is a synthetic cuff placed around the bladder neck & proximal urethra & remains inflated until

intentional deflation by a scrotal or labial pump. 6. Urinary diversion if other measures fail. o Urge incontinence: 1. Augmentation cysto-plasty using bowel segments for patients with over-active bladder refractory

to medical treatment. 2. Sacral neuro-modulation using an electrode permanently stimulating S3 afferent or motor nerves

for patients with over-active bladder or urinary retention refractory to conservative & medical treatment.

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ANDROLOGY

فضائل اجلهاد واالستشهاد يف سبيل اهللامن نن عاب رمرضي اهللا عنهما( ع (ول قال: قالسر الله )لمسو هليع لى اللهإذا: (()ص متعايبت ةينبالع، مذتأخو ابقر أذنالب،

ميتضرع وربالز، مكترتو ادلط ،الجهس الله كمليا علا ذل هزعنى يتوا حجعرإلى ت ينكمد.(( نة أبي عريره )هنع الله يضر( ولأنسر الله ) لى اللهصلمسو هليي(( :قال )عالذو فسن دمحم هدبي! تددي لوو أني أغزف

)).فأقتل أغزو ثم ،فأقتل أغزو ثم ،فأقتل الله سبيل

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MALE INFERTILITY v Definition: o Infertility is the in-ability of a sexually active non-contracepting couple to achieve pregnancy in 1

year. v Incidence: o About 25% of couples (male causes are found in 50%). v Etiology: Causes of spermato-genic failure: 1. Congenital (Anorchia & testicular dys-genesis). 2. Acquired (trauma, torsion, tumour, inflammation (orchitis) & surgery). 3. Mal-descended testes. 4. Chromosomal abnormalities. 5. Systemic diseases (liver cirrhosis & renal failure). 6. Varico-cele. 7. Idiopathic.

IDIOPATHIC MALE INFERTILITY • Therapeutic approaches: o Hormonal:

1. GnRH. 2. HCG/hMG. 3. FSH.

4. Androgens. 5. Anti-estrogens (clomiphene citrate &

tamoxifen-testosterone undecanoate). o Non-hormonal:

1. Kinin-enhancing drugs. 2. Bromocriptine.

3. Anti-oxidants. 4. Mast cell blockers.

VARICOCELE

• Andrological implications: 1. Failure of ipsi-lateral testicular growth & development. 2. Pain & discomfort. 3. Infertility. • Clinical classification: 1. Subclinical: Not palpable or visible at rest or during Valsalva maneuver (detected by special tests as

reflux on Doppler examination). 2. Grade 1: Palpable during Valsalva maneuver. 3. Grade 2: Palpable at rest (but not visible). 4. Grade 3: Palpable & visible at rest. • Diagnosis: Clinical examination & color Doppler. • Treatment: Varico-celectomy by inguinal or high approach (Palomo).

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INVESTIGATIONS • Semen analysis ((1999 WHO criteria)): o Volume: > 2 ml. o pH: 7 - 8. o Sperm concentration: > 20 million spermatozoa/ml. o Sperm count: > 40 million spermatozoa/ejaculate. o Motility: > 50% with progressive motility or 25% with rapid motility within 60 minute after

ejaculation. o Viability: > 50%. o Morphology: > 14% of normal shape & form. o Leukocytes: < 1 million/ml. o Immuno-Bead Test (IBT): < 50% of spermatozoa with adherent particles.

ü Frequency of semen analysis: • If values are normal, 1 test is sufficient. • If values are abnormal in at least 2 tests, further andrological investigation is indicated. § Oligo-zoo-spermia: < 20 million spermatozoa/ml. § Astheno-zoo-spermia: < 50% motile spermatozoa. § Terato-zoo-spermia: < 14% of normal shape & form. ü Quite often, the 3 pathologies occur simultaneously as OAT syndrome. § In extreme cases of OAT syndrome (< 1 million spermatozoa/ml) as in azoo-spermia (no

spermatozoa in semen), there is an ↑ incidence of obstruction of the male genital tract & genetic abnormalities.

ü Causes of azoo-spermia: • Testicular atrophy & agenesis • Obstruction at:

o Rete testis: treated by artificial spermato-cele & ECSI. o Epididymis: treated by vaso-epididymostomy. o Ejaculatory duct (absent fructose in semen): treated by trans-urethral resection.

• Hormonal determinations: o The level of FSH is correlated with the number of spermatogonia. • Testicular biopsy: o For patients without normal FSH & testicular volume to differentiate between obstructive & non-

obstructive azoo-spermia (NOA).

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ERECTILE DYSFUNCTION (ED) v Physiology of penile erection:

• Hemo-dynamics: o Corpora cavernosa: § In the flaccid state, there is tonic contraction of these smooth muscles allowing only a small amount

of arterial flow for nutritional purposes. § Sexual stimulation triggers release of neuro-transmitters from the cavernous nerve terminals →

relaxation of these smooth muscles leading to: 1. ↑ blood flow in both diastolic & systolic phases → dilatation of the arteries & arterioles. 2. Trapping of the incoming blood by the expanding sinusoids. 3. Compression of the sub-tunical venous plexuses between the tunica albuginea & peripheral

sinusoids → ↓ venous outflow. 4. Stretching of the tunica to its capacity which encloses the emissary veins. 5. ↑ intra-cavernous pressure (to about 100 mm Hg) raises the penis from the dependent to the erect

state (full-erection phase). 6. further ↑ (to several hundred mm Hg) with contraction of the ischio-cavernosus muscle → (rigid-

erection phase). o Corpus spongiosum & glans penis: § During erection, the arterial flow ↑ in a similar manner; however, the pressure in the corpus

spongiosum & glans is only 1/3 - 1/2 of that in the corpora cavernosa because the tunical covering is thin over the corpus spongiosum & absent over the glans → minimal venous occlusion.

• Neuro-anatomy & neuro-physiology: 1. Autonomic pathways: o The para-sympathetic pathway is responsible for tumescence. o The sympathetic pathway is responsible for de-tumescence. 2. Somatic pathways: o The pudendal nerve supplies the ischio-cavernosus & bulbo-cavernosus muscles. § Contraction of the ischio-cavernosus muscle → rigid-erection phase. § Rhythmic contraction of the bulbo-cavernosus muscle → ejaculation.

3. Supra-spinal pathways: o The hypo-thalamus & hippocampus are important integration centers for sexual function & erection. o Pathologic processes in these regions such as Parkinson's disease or cerebro-vascular accidents

(stroke) are often associated with ED.

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v Patho-physiology of erectile dys-function: • Incidence: 35% of married men ≥ 60 years old. • Classification: 1. Psychogenic (90%): o Most patents have mixed conditions that may be predominantly functional or physical. 2. Neurogenic: Parkinson's disease, stroke, encephalitis, temporal lobe epilepsy, tumors & dementias. 3. Endocrinologic: o Hypo-gonadism affects libido & sexual behavior. o Hyper-prolactinemia. o Hyper & hypo-thyroidism. 4. Arterio-genic: o Atherosclerotic or traumatic arterial insufficiency (occlusive) disease. ü Risk factors include hyper-tension, hyper-lipidemia, cigarette smoking, diabetes mellitus, blunt

perineal or pelvic trauma & irradiation. 5. Veno-genic (Cavernosal): o Failure of adequate venous occlusion (one of the most common causes of vasculo-genic impotence). o Degenerative changes (Peyronie's disease, old age & diabetes mellitus). o Traumatic injury to the tunica albuginea (penile fracture). o Acquired venous shunts. 6. Drug-induced: 1. Sympatho-lytics (e.g. methyldopa & clonidine). 2. α-adrenergic blockers (e.g. phenoxy-

benzamine & phentolamin). 3. Β-adrenergic blockers.

4. Thiazide diuretics & spironolactone. 5. Alcohol in large amounts. 6. Cimetidine.

• Diagnosis: 1. Neurological examination. 2. Nocturnal penile tumescence test (normally erection occurs 3-5 times during sleep). 3. Duplex US to study penile arterial & venous systems. 4. Internal pudendal arterio-graphy. • Treatment: 1. Behavioral sex therapy. 2. Vacuum erection device: placed around the penis to create -ve pressure for erection & its

constriction ring maintains erection. 3. Penile prostheses. 4. Intra-cavernous injection of alprostadil (PGE2), papaverine & phentolamine. 5. Drugs:

o Trans-urethral alprostadil. o Oral phospho-di-esterase inhibitors as sildenafil (viagra), vardenafil & tadalafil.

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