Surgery part 3 pdf - د.أحمد

Lec:11

Surgery

Advances in the Management of BPH

The Scale of the Problem



Moderate to severe Lower Urinary Tract Symptoms (LUTS) occur in 25% of men over 50
years, and the incidence rises with age



Approximately 90% of men will develop histological evidence of BPH by 80 years of age

Increasing because:-

1.  Men are living longer
2.  Proportion of Men over 50 years will increase
3.  Men are better informed about health matters

Difficulties in Diagnosis and Management



The symptoms of BPH are the same as those of early Prostate Cancer



Confirmation of the presence of prostate cancer may be difficult



The need to treat (proven) cancer may not always be clear cut

Understanding Lower Urinary Tract Symptoms (after Abrams, Bristol, UK)

Storage Symptoms



Frequency



Nocturia



Urgency



Urge incontinence



Bladder Pain

Voiding Symptoms



Slow stream



Intermittent flow

Detrusor Instability

Bladder Hypersensitivity

Bladder Outlet Obstruction

Detrusor Failure



Hesitancy



Straining



Terminal dribble

Physical Signs



May be few



Look for obvious uraemia



Palpate for full bladder



Examine urethral meatus and palpate urethra for stricture



DIGITAL RECTAL EXAMINATION (DRE) !!

Investigations for BPH



Urea and electrolytes if clinically indicated



PSA (should we counsel patients?)



Ultrasound urogram



Flow rate (if you have access)



IPSS

IPSS

A word about Prostate Cancer



No symptoms specific for early prostate cancer



Presenting symptoms are therefore those of BPH



Biopsy of the prostate should be performed in those with abnormal DRE, or PSA
above age-specific reference range

Prostate Specific Antigen



Single-chain glycoprotein of 240 aa residues and 4 carbohydrate side chains



Physiological role in lysis of seminal coagulum



Prostate specific, but NOT cancer specific

In addition to prostate cancer, an elevated level may be found in



Increasing age



Acute urinary retention / Catheterisation



after TURP / Prostate Biopsy



Prostatitis



BPH

A reduced level may be found in patients treated with Finasteride

The Problem with PSA



Men with Prostate Cancer may have a normal PSA



Men with BPH or other benign conditions may have a raised PSA



May not even be prostate-specific!



What to do with men with a PSA of 4-10 ng/ml



PSA = Persistent Source of Anxiety

Refinements in the use of PSA



PSA density



PSA Velocity



Age-Specific PSA

40-49 Years old

<2.5ng/ml

50-59 Years old

<3.5ng/ml

60-69 Years old

<4.5ng/ml

70-79 Years old

<6.5ng/ml



Free:Total PSA ratio (<0.15 strongly suggests possibility of Ca

Prostate)

Prostate Specific Antigen



Possibly



Some



Attributes

The Management of BPH

Advances in the Management of BPH

New treatment modalities for BPH



-blocker therapy (including selective blockers of



-1a receptors)

2. 5-



-reductase inhibitors - Finasteride (Proscar)

3. Minimally invasive Techniques

o  Transurethral Microwave Thermotherapy (TUMT)
o  Transurethral Needle ablation (TUNA)
o  Transrectal high-intensity focused ultrasound (HiFU)
o  Transurethral electrovaporisation (TUVP)

1. Alpha blocker therapy

2. Finasteride (Proscar) - PLESS study has confirmed that men with large prostates

(>40cc), taking long-term therapy, less likely to develop acute retention, or require
surgical intervention

3. Minimally invasive therapies



High energy TUMT, and TUNA, have proven clinical efficacy between that of drug
therapy and TUVP or laser therapy



HiFU currently requires GA, is costly and time consuming, and appears unlikely to
be popular at present



The subjective response after MITs and TURP appear similar, but objective results
superior for TURP

Surgical Therapies



TURP still the gold standard therapy, with which all other therapies must be
considered



Laser therapy

o  expensive to set up
o  Significantly reduced blood loss
o  Catheter may be required post operatively



Open Prostatectomy rarely required

Guidelines for the Management of BPH



Produced after discussion between working party of General Practitioners and
Consultants



Agreed within the department of Urology

Protocol for the management of BPH

Eligible for Shared Care

Prostate Clinic

Normal

DRE and PSA

Outpatient appt with

Consultant

Abnormal

DRE and PSA

Referral to Urology Department

Management by GP

(See next slide)

Options

Flow rate and Residual volume if possible

History

IPSS Score

DRE

U+E and PSA

GP Assesses Patient

Future perspectives for the management of BPH



Much more emphasis on Quality of Life



Minimally invasive therapies are improving and may yet challenge the superiority of
TURP

Conclusions - BPH



Remains an important cause of patient morbidity



Correct approach to assessment is important



Many men may have their symptoms relieved by alpha blocker therapy or Finasteride,
which has also been shown to reduce the likelihood of surgery or acute urine
retention



A large variety of MITs exist for BPH who fail drug therapy, but for most patients the
gold standard surgical procedure remains TURP



The next few years will see many more techniques available to challenge the position
of TURP

Severe

IPSS > 20

Flow rate < 10 mls/s

Resid vol > 200 mls

Moderate

IPSS 7-20

Flow rate < 15mls/s

Resid vol <200 mls

Mild

IPSS<7

Flow Rate >15 mls/s

Resid vol < 100 mls

IPSS Score

Refer to the Urology

Department

alpha-blockers:

Refer if no improvement

Watchful Waiting

Management

Lec:12

Surgery

Prostate Carcinoma



Prostate cancer is the most common cancer diagnosed and is the second leading cause

of death



The prevalence of cancer increase with age, the probability of Ca P developing

in men under age of 40 is 1/10.000, for men 40-59 it is 1/103, 60-79 it is 1\8.



Blacks are at higher risk than whites.



Positive family history of CaP increase RISK of CaP.



High dietary fat intake increase the relative risk of CaP.

Etiology



The gene responsible for familial Ca P resides on chromosome 1



The region most commonly identified are chromosome 8p, 10Q, 13Q, 17P and 18Q.



Epithelial stromal interaction under the influence of growth factors Such as :

1.  Transforming growth factors –B.
2.  Platelets-derived growth factor.
3.  Neuroendocrine peptide.

Pathology



Over 95% of CaP are adenocarcinoma



Of 5% : 90% Transitional cell carcinoma

Neuroendocrine carcinoma

Sarcoma

The cytological characters of CaP include:



Hyperchromatic, enlarged nuclei, with prominent nucleoli.



Cytoplasm is often abundant, blue-tinged or basophilic.



The basal cell layer is absent in CaP, it is present in normal gland.



Prostatic intraepithelial neoplasia (PIN) is the precursor to invasive CaP.



The distinguishing feature of invasive CaP is that the basal Cell layer is absent.



60 -70% of CaP originate in the peripheral zone.



10- 20% transition zone.



5-10% central zone.

Grading and Staging

TNM Staging System

Gleason grade



Gleason grade range from 1 to 5, gleason score range from 2 to 10.



Well differentiated tumor have a gleason score of 2-4.



Mod differentiated tumor 5-6.



Poorly differentiated tumor 8-10.



Gleason score of 7 is grouped with mod differentiated tumor.



Gleason grade 1 and 2 characterized by small uniformly shaped gland, with little

intervening stroma.



Gleason grade 3 characterized by variable sized gland.



Gleason grade 4 has a several histologic appearance.



Gleason grade 5 has single infiltrating cell, no gland formation.



Comedocarcinoma is a variant of gleason grade 5.

Whitmore-Jewett

Clinical

Picture

Symptoms:



Most patient are asymptomatic in early stage.



Obstructive and irritative voiding symptoms can result from Local growth pf tumor

(urethra, bladder neck).



Bone pain in metastatic disease.



Symptoms of spinal cord compression (paresthesia, weakness, urinary and fecal

incontinence).

Signs:



DRE: induration.



Lympadenopathy.



Lymphedema.



Signs of metastases.

Lab Findings:



Azotemia.



Anemia.



Alkaline phosphatase elevated in bone metastasis.



Acid phosphatase.

Tumor Markers



PSA.



Prostate biopsy is the most commonly employed technique.



Increase the sensitivity of cancer detection.



Indicated in elevated PSA, abnormal DRE.

Imaging



TURS: useful in performing prostate biopsy.



Provide local staging.



Measure prostate volume.



CT scan confirm local or distant metastasis.



MRI.



Bone scan is the standard part of initial evaluation.

Molecular staging



Detection of circulating CaP cells in peripheral blood.



By using (RT-PCR) revers transcription-polymerase chain reaction).

Differential Diagnosis

Not all patients with elevated PSA have prostate cancer as it elevates in:

1.  BPH.
2.  Urethral instrumentation.
3.  Infection.
4.  Prostatic infarction.
5.  Prostate calculi.
6.  Alkaline phosphatase increase also in Paget disease.

Pattern of progression



Local extension outside the prostate (extra capsular extension) or seminal vesicle

invasion and distant metastasis increase with increase tumor volume.



Small and well differentiated cancer usually confined to prostate



Large volume and poorly differentiated (G 4-5)>4cm often locally extensive, metastatic

to lymph node or bone.



Locally advanced CaP invade bladder trigone, lead to ureteral obstruction.

Lymphatic metastases most identified to:



Obturator lymph node, common iliac, presacral and periaortic.



The axial skeleton is the most usual site of distant metastases (Lumbar spine, femur,

thoracic spine, Ribs, sternum, skull) can lead to pathologic fracture.



Visceral metastases (lung, liver, adrenal gland).

Diagnosis



DRE.



PSA.



TRUS.



Prostate biopsy.



Grading and staging.

Treatment

Localised Disease



Radical prostatatectomy: provide removal of prostate, seminal vesicle,block dissection

of obturator and ext iliac lymph node.



Radiation therapy.



Cryosurgery.

Locally advanced disease



Radiation therapy also indicated in unfit patient and symptomatic metastases (it leads to

relief of pain).



TUR: in patients with urinary outflow obstruction.



Bil Orchidectomy.

Hormonal Therapy:



Is the main line of treatment in metastases disease.



Is used in unfit patient for surgery or radiotherapy.



Bilateral orchidectomy (removal of testicular tissue).

LHRH agonist (zoladex)
It causes initial rise in testosterone level for (4-6) weeks then drop to castration level.

Antiandrogen (block testosterone receptors)
It is used as adjuvant therapy.

Prognosis



Organ confined cancer, 10 years free survival range 70-85%.



Focal extracapsular extension, free survival 70% at 5 years 40% at 10 years.



High grade, free survival 15%at 10 years.

Lec:13

Surgery

Scrotal Pathologies

Anatomy

Incompletely descended testis (Undescended Testis):

The testis is arrested in some part of its path to the scrotum.



Incidence: 4% of boys are born with one or both testes incompletely descended.



Half of these reach the scrotum during the first month of life.



two thirds of these reach the scrotum during the first three months of life



incidence of testicular maldescent at the age of one year is around 1 per cent



In 10% of unilateral cases there is a family history.

Pathology



The epithelial elements are immature histologically and by late puberty irreversible
destructive changes halt spermatogenesis and limit the production of androgens.



Early repositioning of an incompletely descended testis can preserve function

Clinical features



The scrotum is empty & underdeveloped



More common on the right



Bilateral in 20% of cases.



Secondary sexual characteristics are typically normal.

The testis may be:



intra-abdominal, lying extraperitoneally above the internal inguinal ring.



inguinal, it may or may not be palpable



in the superficial inguinal pouch, in which case it must be distinguished from retractile
testis.

Hazards of incomplete descent



Sterility in bilateral cases (especially intra-abdominal testes)



Pain as a result of trauma



Indirect inguinal hernia often present



Torsion of the testis



Epididymo-orchitis



Atrophy of an inguinal testis before puberty may possibly be caused by recurrent
minor trauma



Testicular cancer is more common in an incompletely descended testes

N.B. orchidopexy may or may not diminish the risk of testicular cancer but it does improve
the prospect of early diagnosis .

Treatment



Orchidopexy is usually performed after the age of one year



The testes should be brought down into the scrotum before the boy starts school.



Orchidectomy should be considered if the incompletely descended testis is atrophic



Hormone treatment with human chorionic gonadotrophin is appropriate only when
there is established hypogonadism.

ECTOPIC TESTIS

The testis is abnormally placed outside this path

The sites of ectopic testis are:

•  at the superficial inguinal ring: superfecial to the inguinal canal
•  the perineum
•  the root of the penis
•  the femoral triangle.

An ectopic testis is usually fully developed. The main hazard is liability to injury.

Treatment: orchidopexy

N.B.: Retractile testis is normal testis with active cremasteric reflex

INJURIES TO THE TESTIS



Blunt or penetrating trauma



Contusion and rupture of the testis are associated with a collection of blood around
the testis and cannot usually be distinguished with certainty without exploration.



O/E: scrotal swelling, bruises, Loss of testicular contour



U/S is the investigation of choice



Haematocele ( collection of blood between two layers of tunica vaginalis) should be
drained and the tunica albuginea repaired after evacuation of haematoma.



A severely damaged testis may have to be removed.

ABSENT TESTIS



‘Vanishing’ testis: a condition in which a testis develops but disappears before birth.



Cause: prenatal torsion.



True agenesis of the testis is rarer.



Laparoscopy is useful in distinguishing these causes of clinically absent testis from
intra-abdominal maldescended testis.

Scrotal Swelling

Scrotal swelling with pain:



Epididymitis



Orchitis



Testicular trauma



Testicular torsion



Incarcerated scrotal hernia



Testicular tumor

Scrotal Swelling without pain:



Hydrocele



Spermatocele



Varicocele



Hematocele



Scrotal hernia



Testicular tumor

TORSION OF THE TESTIS ( Torsion of spermatic cord)



Rotation of the testis around the vertical axis of the cord



It is time limited due to arterial obstruction & the patient might lose his testis by
ischemia (gangrene) if the diagnosis is delayed (6 hours).



It may develop spontaneously during sleep.



Straining at stool, lifting a heavy weight, trauma, and coitus are all possible
precipitating factors.

Clinical features



Most common between 10 and 25 years of age



Sudden agonizing pain in the groin and the lower abdomen.



The patient feels nauseated and may vomit.



The testis lie transversely high and the tender twisted cord can be palpated above it.



Testicular elevation does not relief pain



Loss of cremasteric reflex

Diagnosis

Doppler ultrasound scan will confirm the absence of the blood supply to the affected testis

Treatment



Exploration for torsion



If the testis is viable when the cord is untwisted then it is fixed (orcheopexy).



An infarcted testis (gangrenous) should be removed (orchidectomy).



The other testis should also be fixed because the anatomical predisposition is likely to
be bilateral.

N.B: In the first hours it may be possible to untwist the testis manually, then early
orcheopexy to avoid recurrent torsion

VARICOCELE

It is a varicose dilatation of the veins draining the testis ( abnormal dilatation of the
pampiniform plexus)
Most varicoceles present in adolescence or early adulthood
Usually on the left.

Clinical Features

Usually symptomless
There may be dragging scrotal discomfort
The scrotum on the affected side hangs lower than normal
On palpation, with the patient standing, the varicose plexus feels like a bag of worms.
Infertility ?

Investigations:

Scrotal Doppler U/S

Treatment

Operation is not indicated for asymptomatic varicocele.
Indicatioins: pain, infertility, cosmetic
Types of operations:

•  Varicocele ligation
•  laparoscopic ligation
•  Embolisation of the testicular vein under radiographic control

HYDROCELE

Hydrocele is an abnormal collection of serous fluid in a part of the processus vaginalis,
usually the tunica.
Vaginal hydrocele abnormal collection of serous fluid between the two layers of tunica
vaginalis.
In congenital hydrocele, the processus vaginalis is patent and connects with the peritoneal
cavity.

Etiology

Acquired hydroceles are primary (idiopathic), or secondary to testicular disease.
A hydrocele can be produced in four different ways
• by excessive production of fluid within the sac, e.g. secondary hydrocele

• by defective absorption of fluid; this appears to be the explanation for most primary
hydroceles although the reason why the fluid is not absorbed is obscure
• by interference with lymphatic drainage of scrotal structures
• by connection with the peritoneal cavity via a patent processus
vaginalis (congenital).

Clinical features

Primary vaginal hydrocele is most common in middle and later life but can also occur in
older children presents with scrotal swelling
Painless
Typically translucent (transillumination +ve)
It is possible to ‘get above the swelling’ on examination of the scrotum
N.B: in a young man; there may be a testicular tumour, so scrotal US should be done.

Treatment

Congenital hydroceles are treated by herniotomy if they do not resolve spontaneously
Acquired hydroceles: excision of the wall

N.B: A secondary hydrocele may subsides when the primary lesion resolves.

Epididymal cysts

They represent cystic degeneration of the epididymis.
Filled with a crystal-clear fluid.
Found in middle age
The cysts are multilocular
Excision may cause obstruction of the epididymis therefore it is better to leave it.

Spermatocele

A unilocular retention cyst derived from some portion of the sperm-conducting mechanism
of the epididymis.
Typically lies in the epididymal head above and behind the upper pole of the testis.
The fluid contains spermatozoa
Small spermatoceles can be ignored. Larger ones can be aspirated or excised through a
scrotal incision.

EPIDIDYMO-ORCHITIS

Inflammation confined to the epididymis is epididymitis
Infection spreading to the testis is epididymo-orchitis.

Acute epididymo-orchitis

Mode of infection

Infection reaches the epididymis via the vas from a primary infection of the urethra,
prostate or seminal vesicles

Blood-borne infections of the epididymis are less common
N.B: Acute epididymo-orchitis can follow any form of urethral instrumentation. It is
particularly common when an indwelling catheter is associated with infection of the
prostate.

Clinical features

The initial symptoms are those of urinary tract infection.
The epididymis and testis swell and become painful.
Fever
The scrotal wall, at first red, oedematous and shiny, may become adherent to the
epididymis.
Resolution may take 6–8 weeks to complete.
Occasionally, an abscess may form and discharge of pus through the scrotal skin.
N.B: Acute epididymo-orchitis develops in about 18% of males suffering from mumps.
The main complication is testicular atrophy, which may cause infertility if the condition is
bilateral.

Investigations

GUE
Urine C&S
WBC count
Scrotal U/S

Treatment

Broad spectrum antibiotics for 2 weeks (3

generation cephalosporin or quinolones)

Scrotal support
Supportive therapy (analgesics, antipyretics, anti emetics, IVF)
If suppuration occurs(Abscess): drainage is necessary.

TUMOURS OF THE TESTES

•  Most testicular neoplasms are malignant
•  It is one of the most common forms of cancer in young men.
•  Maldescent  predisposes to malignancy
•  The lymphatic drainage of the testes is to the para-aortic lymph nodes near the origin

of the gonadal vessel.

• The inguinal lymph nodes are affected only if the scrotal skin is involved.

Classification

They are classified according to their predominant cellular type:

1. GCTs:

o Seminoma (40%):

The enlarged testis is smooth and firm.
metastasize via the lymphatics.
Hematogenous spread is uncommon.

o Nonseminomatous GCT or Teratoma (32%):

Arises from totipotent cells in the rete testis and often contains a variety of cell
types, of which one or more predominate.
They may secrete human chorionic gonadotrophin (HCG) & alpha-fetoprotein.

o Combined seminoma and teratoma (14%)

2. Interstitial tumours (1.5%):

arise from Leydig or Sertoli cells

3. Lymphoma (7%)
4. Other tumours (5.5%)

Clinical features

•  testicular lump which is usually painless
•  sensation of heaviness occurs when the testis is two or three times its normal size
•  The testis is enlarged, smooth, firm and heavy
•  Secondary hydrocele
•  Secondary retroperitoneal deposits may be palpable, just above the umbilicus,

hepatic enlargement, enlarged supraclavicular nodes

• Symptoms of metastatic disease: abdominal or lumbar pain, chest pain, dyspnoea

and haemoptysis

• Rarely, patients present with severe pain and acute enlargement of the testis because

of haemorrhage into a neoplasm

Between 1% and 5% of cases have gynaecomastia (mainly the teratomas).

Investigations

•  Tumour markers (HCG, alpha-fetoprotein and lactate dehydrogenase)
•  U/S scanning of the testis
•  CXR: pulmonary metastases especially in teratoma

CT scan and MRI are the most useful means of detecting secondaries and of monitoring the
response to therapy.

Staging

Treatment

Radical orchidectomy through inguinal approach.

Further Mx:

Further treatment depend on staging and histological diagnosis (after orchidectomy):

Seminomas

Radiosensitive

Highly sensitive to cisplatin, which is used for patients with metastatic disease.

Teratomas

less sensitive to radiation

Chemotherapy:

Cisplatin, methotrexate, bleomycin and vincristine : used in combination with great

success.

For both seminoma & teratomas: Retroperitoneal lymph node dissection is sometimes
needed when retroperitoneal masses remain after chemotherapy

Prognosis

Seminoma: the 5 years survival after orchidectomy and radiotherapy or chemotherapy:

If there are no metastases 95%.
If there are metastases 75%

Teratoma: 5-year survival rate:

stage 1 - 2: of more than 85%
stage 3 - 4 : about 60%

Idiopathic scrotal gangrene- Necrotizing fasciatis (Fournier’s
gangrene)

Fulminating inflammation of the subcutaneous tissues, which results in an obliterative
arteritis of the arterioles to the scrotal skin
Most commonly occurs in immunocompromised patients

Causative organisms:

mixed infection of Haemolytic streptococci (sometimes

microaerophilic), Staphylococcus, E. coli, Clostridium welchii.

Clinically:

Sudden scrotal inflammation
Rapid onset of gangrene and loss of scrotal skin leading to exposure of the scrotal contents
The absence of any obvious cause in over half the cases.

The condition can follow minor injuries or procedures in the perineal area, such as a bruise,
scratch, urethral dilatation, injection of haemorrhoids or opening of a periurethral abscess.

Clinical features

Sudden pain in the scrotum, prostration, pallor and pyrexia.
Cellulitis spreads until the entire scrotal coverings slough, leaving the testes exposed but
healthy

Treatment

The microorganisms are usually sensitive to gentamicin and a cephalosporin
Wide excision of the necrotic scrotal skin
Many patients die despite active treatment

Vesicoureteral reflux (VUR )

Definition:
VUR results from abnormal retrograde flow of urine from the bladder into the upper urinary
tract.
It is caused by primary or secondary incompetence of the ureterovesical valve mechanism.

Epidemiology

•  Overall incidence in children is >10%
•  Asymptomatic children have an incidence of 17%
•  VUR is present in 70% of infants with urinary tract infection.
•  More importantly, between 30% and 50% of children with reflux will have renal

scarring.

• Reflux is the second most common cause of prenatal hydronephrosis and accounts for

37% of cases.

•  Adults with urinary tract infection (UTI) have a 5% incidence of reflux.
•  Younger children affected more than older children
•  Girls more than boys (female–male ratio 5:1)
•  VUR occurs more often in Caucasian than in Afro-Caribbean children.
•  Siblings of an affected child have a 40% risk of reflux, and routine screening of siblings is

recommended.

Pathogenesis

• The ureter passes obliquely through the bladder wall (1–2 cm), where it is supported by

muscular attachments that prevent urine reflux during bladder filling and voiding.

•  The normal ratio of intramural ureteric length to ureteric diameter is 5:1.
•  Reflux occurs when the intramural length of ureter is too short (ratio <5:1).
•  The appearance of the ureteric orifice changes with increasing severity of reflux,

classically described as stadium, horseshoe, golf-hole, or patulous.

Classification

Primary reflux (1%) results from a congenital abnormality of the ureterovesical junction.
Secondary reflux results from urinary tract dysfunction associated with elevated intravesical
pressures.

Etiology

1. Primary reflux is caused by lateral displacement of the ureteral orifice during

embryogenesis and a shorter intramural tunnel for the ureter, resulting in a poor
muscular backing. A weaker valve mechanism is therefore available to close the orifice
during bladder contractions.

2. Ureteral duplication is commonly associated with reflux into the lower pole ureter, again

owing to its abnormally short intramural tunnel.

3. Ureteral ectopia without ureterocele may be associated with reflux.
4. Abnormalities of the bladder wall such as diverticula, radiation cystitis, and
cyclophosphamide cystitis may predispose to vesicoureteral reflux. UTI may be associated
with transient reflux, due to the inflamed bladder wall.
5. Elevated intravesical pressure from any cause may lead to reflux. Common causes are
posterior urethral valves, detrusor hyperreflexia, and prostatic enlargement in adults.
6. Prune-belly syndrome is a congenital condition characterized by deficient anterior
abdominal musculature, bilateral cryptorchidism, bilateral megaureter, and often bilateral
vesicoureteral reflux.
7. Iatrogenic reflux may result from any surgical procedure that disrupts the trigonal
muscle, such as prostatectomy. Resection of the ureteral orifice can also produce reflux.
8. Dysfunctional voiding or elimination syndromes can lead to reflux. Voiding patterns
should always be elicited in the medical history.

Grading of VUR

• The degree of reflux is graded I–V.

• Grading is based on the appearance of contrast agent in the collecting system during

voiding cystourethrography (VCUG(.

Complications

Presentation

Vesicoureteral reflux rarely causes symptoms.
Most patients present as recurrent UTI or pyelonephritis: have symptoms of fever, dysuria,
suprapubic or abdominal pain, failure to thrive, vomiting, and diarrhea.
In more advanced stages, the patient may present with uremia or hypertension.

Investigations

Urinalysis and culture to diagnose UTI
Urinary tract ultrasound scan to diagnose reflux
The VCUG:

the definitive examination
to diagnose and grade reflux and establish reversible causes
must include a voiding phase:

in some cases, reflux may be seen only during the elevated intravesical
pressures associated with micturition.
in visualizing the urethra, may allow the diagnosis of outflow obstruction to be
made (e.g., posterior urethral valves).

DMSA scan to detect and monitor associated renal cortical scarring.
The intravenous urography (IVU) findings are usually normal in lower grades of reflux.
Urodynamic assessment if suspicious of voiding dysfunction
Cystoscopy: to study position and morphology of ureteric orifices and exclude secondary
causes.

Management

• Correct underlying problems contributing to secondary reflux.
• Depending on:

o  the grade of reflux as determined by VCUG
o  the age of the patient at diagnosis
o  unilateral versus bilateral disease

• Most primary VUR grade I–II cases will resolve spontaneously (~85%), with 50%

resolution in grade III.

• Observation and medical treatment are initially recommended.

Medical management
• Low-dose antibiotic prophylaxis should be given to keep the urine sterile and lower the

risk of renal damage until reflux resolves.

o Indicated in cases of low-grade vesicoureteral reflux without outlet obstruction

or another abnormality.

o Good patient compliance is necessary.
o Long-term antibiotic suppression with a regimen of amoxicillin (neonate),

trimethoprim/sulfamethoxazole, nitrofurantoin, or other antibiotic agent at one-
fourth to one-half the usual dose daily is commonly used.

• Anticholinergic drugs are given to treat bladder overactivity.

Medical management

If the patient remains asymptomatic, urine cultures are obtained periodically (e.g., every 3
months) during treatment. US and radionuclide cystogram should be obtained at yearly
intervals.
If acute (breakthrough) infection occurs, a full course of appropriate antibiotics is given and
a prophylactic regimen is then instituted.
Clinicians perform a dimercaptosuccinic acid scan (DMSA) to look for renal scarring at this
juncture.
Surgery is often recommended after breakthrough UTI.

Resolution of vesicoureteral reflux with antibiotic prophylaxis

•  G1= 90%
•  G2= 60%
•  G3= 50%
•  G4= 30%
•  G5= 0%

Surgical therapy

• Indicated in patients with:

o  high-grade primary reflux (grades 4 and 5)
o  those with low-pressure reflux and significant hydroureter
o  persistant reflux in girls after puberty
o  patients in whom medical management has failed:

  persistence of reflux after 3 to 4 years of antibiotic prophylaxis
  multiple breakthrough infections
  new or increased renal scarring
  deterioration of renal function
  noncompliance with medication

• Techniques of ureteral re-implantation include the following:

o Intravesical methods involve mobilizing the ureter and advancing it across the

trigone (Cohen repair) or reinsertion into a higher, medial position in the
bladder (Politano–Leadbetter repair(

o Extravesical techniques involve attaching the ureter into the bladder base and

suturing muscle around it (Lich–Gregoir procedure(

• Has a 98% cure rate.

• Approximately 1% of patients have obstruction of the ureterovesical junction after

ureteral reimplantation that requires reoperation.

• In patients with massive ureteral dilatation, tapering of the distal ureter may be

necessary during reimplantation.

• Rarely, temporary supravesical diversion is necessary in patients who are severely

uremic.

• Alternatively, endoscopic subtrigonal injection of Deflux into the ureteral orifice has

70% success, and 95% with repeated treatments.

Lec:14

Surgery

ANDROLOGY (Erectile Dysfunction)

Goals and Objectives



Define erectile dysfunction (ED)



Discuss the most common causes of ED



Review a practical evaluation of men with ED



Review the treatment options



Provide suggestions for urologic referral

What is ED?

ED is the inability to achieve and maintain an erection adequate for intercourse to the
mutual satisfaction of the man and his partner.

Remember, both partners in a relationship are affected.

Incidence



20-30 million American men suffer ED



Age dependent

o  2% men age <40 years
o  25% men age 65
o  75% men >75 years



Not a necessary occurrence of the aging process

How Does an Erection Occur?



The brain controls all sexual functions, from perceiving arousal to initiating and
controlling the psychological, hormonal, nerve, and blood flow changes that lead to an
erection.



Hormones, including testosterone, control the male sex drive



Nerve impulses relay signals of arousal and sensation to and from the penis



Arteries deliver extra blood to the penis that causes it to stiffen.



Veins then drain the blood out of the penis after intercourse.

Physical or Psychological Stimuli Results



Sacral parasympathetics (S2,3,4) stimulation to the penile nerves



Dilation of the penile arteries



Relaxation of the smooth muscle in the corporal bodies of the penis



Decrease venous outflow

An Erection Requires a Coordinated Interaction of Multiple Organ Systems



Psychological



Endocrine



Vascular



Neurologic

Mechanism of Smooth Muscle Relaxation



Release of Neurotransmitters-nitric oxide



Conversion of GTP to cGMP - erection



Breakdown of cGMP by PDE type 5 - detumesence

Cause of ED



Psychogenic Causes:

o  Anxiety
o  Depression
o  Fatigue
o  Guilt
o  Stress
o  Marital Discord
o  Excessive alcohol consumption



Organic Causes

o  Cardiovascular disease
o  Diabetes mellitus
o  Surgery on colon, bladder, prostate
o  Neurologic causes (lumbar disc, MS, CVA)
o  Priapism
o  Hormonal deficiency

Risk Factors
Massachusetts Male Aging Study (Feldman Ha, J Urol 1994; 151:54-61)



Treated heart disease

39%



Treated diabetes

28%



Treated hypertension

15%

Other risk Factors (Benet et al. Urol Clinic North Am. 1995; 151:54-61)



Diabetes

27% - 59%



Chronic renal failure

40%



Hepatic failure

25% - 70%



Multiple Sclerosis

71%



Severe depression

90%



Other (vascular disease, low HDL, high cholesterol)

Causes of ED



Hormone Deficiency



End Organ Failure



Blockage of Blood Vessels



Venous Leak



Spinal cord injuries: 5% - 80%



Pelvic and urogenital surgery and radiation



Substance abuse



Alcohol: >600ml/wk



Smoking amplifies other risk factors



Medications may be responsible for ~25% of cases of ED



Bicycle riding



Medication:

o  Most common cause of ED in men >50
o  Many men are polymedicated
o  Also have co-morbid conditions
o  Anti-hypertensive drugs

  All capable
  Common: thiazides and beta blockers
  Uncommon: calcium channel blockers, alpha-adrenergic blockers, and ACE

inhibitors

o CNS drugs:

 Antidepressants, tricyclics, SSRIs

  Tranquilizers
  Sedatives
  Analgesics

o  H1 and H2 receptor blockers
o  Anticholinergics
o  LHRH agonists (Lupron, Zolladex)
o  Alcohol
o  Tobacco
o  Drug abuse
o  Estrogens, Ketoconazole

A Practical Evaluation of Men with ED

#Basic evaluation



Medical History



Cardiovascular history



Endocrine history



Sexual history/questionnaire



Physical exam:

o  Focused neurovascular exam
o  Size of testis
o  DRE



Lab tests

o  UA
o  Testosterone, CMP, Lipid panel
o  PSA in men >50 years

#Sexual History



Premature ejaculation



Retarded ejaculation



Painful intercourse



Anorgasmia



Decreased Libido



Dissatisfaction with sex life



Do you have any problems with intimacy with your partner?



Do you have early morning erections?



Do you have erections with self-stimulation?



Are you able to consistently obtain and maintain an erection sufficient for sexual
intimacy?



Does it hurt to have an erection or intercourse?



Do you ejaculation sooner than you would like?



Does it take too long to reach an orgasm?



Do you fail to reach an orgasm?



Did your erection problems start suddenly or over time?

#ED Questionaire³



When you had erections with sexual stimulation, how often were your erections hard
enough for penetration?



How do you rate your confidence that you could get and keep an erection?

³The International Index of Erectile Function, Urol 1997;49:822-830



During sexual intercourse, how often were you able to maintain your erection after you
had penetrated your partner?



During sexual intercourse, how difficult was it to maintain your erection to completion
of intercourse?



When you attempted sexual intercourse, how often was it satisfactory for you?

#Differentiating Psychogenic from Organic ED

Psychogenic Impotence:



Younger patient (<40)



Preservation of morning erections and nocturnal erections



Achieve erection with masturbation



May be partner-specific



Often sudden onset

Organic ED:



Gradual deterioration



Decrease in morning erections and nocturnal erections



No erections with masturbation



No loss of libido



Presence of co-morbid conditions

#Physical Examination



Blood pressure



Examine penis (R/O Peyronie’s disease)



Determine size and consistency of testes



Digital rectal exam



Focused vascular exam/peripheral pulses



Focused neurologic exam

#Laboratory Tests



UA (glycosuria) – Fasting if elevated



PSA in men over 50



Testosterone (best to draw in A.M.)



Prolactin, Thyroid function, Lipid profile, Liver function, Creatinine

#Other Tests



NPT – Nocturnal Penile Tumescence Test



Penile doppler



Injection of vasoactive drugs



NEVA (Nocturnal Electobioimpedance Volumetric Assessment)

Treatment Options

#Goal directed therapy



Find out what the patient wants



Try to tailor the treatment to the patients needs and wants



Etiology rarely affects treatment choice for the patient



Nonpharmacologic



Non-invasive



Minimally invasive



Invasive



Counseling and/or sex therapy



Oral medications - Viagra, Levitra, Cialis



Urethral suppositories (MUSE)



Injection therapy - Caverject, Trimix, Bimix



Vacuum constriction device



Surgery



Sex therapy

#Counseling and/or Sex Therapy



Rule out depression



Try oral medication in patient with psychogenic impotence



Refer to sex therapist or psychiatrist for sever psychopathology

#Nonpharmacologic Treatment Options

Lifestyle changes:



Reduce fat and cholesterol in diet



Decrease or limit alcohol consumption



Eliminate tobacco use and substance abuse



Weight loss if appropriate



Regular exercise

#Ideal Medication for Treatment of ED



Effective



Available on demand



Free of toxicity and side effects



Easy to administer



Inexpensive

#Medication

(Viagra, Levitra, Cialis)

Mechanism of Action:



PDE inhibitor and increases the cGMP that promotes and sustains smooth muscle
relaxation

(PDE Inhibitors)

Indications:



Psychogenic ED



Mild vasculogenic ED



Neurogenic ED



Side effects from medication(s) patient is already taking

Side effects:



Headache



Flushing



Dyspepsia



Nasal congestion



Visual disturbances



Priapism

Contraindications:



Organic Nitrites:

o Oral
o Sublingual



Severe cardiac disease

o Obtain stress testing

(Yohimbine, Yocon, Erex, Yohimex)



Alpha 2 andrenoreceptor antagonist



Dose: 5.4 mg TID



Results: ~20% (same as placebo)



Side effects: increase blood pressure, tachycardia, anxiety

Trazodone(Desyrel)



Anti-depressant associated with priapism



Mechanism of action nor fully understood



Nor FDA approved for ED



Side effects: drowsiness, dry mouth, sedation, priapism

Apomorphine (Spontane)



Dopaminergic mechanism with hypothalamic activity



Sublingual administration



64% to 67% response rate with ED



Side effects: nausea, sweating, hypotension, yawning



Awaiting FDA approval

Phentolamine (Vasomax)



Alpha-blocker



Relaxes smooth muscle tissue



40% efficacy in mild organic ED



Side effects: nasal congestion, tachycardia, dizziness, hypotension



Awaiting FDA approval

Side effects



Discontinue tobacco, alcohol, and abusive drugs



Alter dosage of drugs with ED side effects



Change to another class of drugs

Transurethral Therapy (Alprostadil – MUSE)



Mechanism of Action: vasodilator



Administration: 125, 250, 500. 1000ug



Insert in the urethra



Erection occurs 10-15 minutes later



Erection lasts 30-45 minutes



Results: 10-65%



Side effects: Pain, bleeding, priapism (<3%)

Penile Injection Therapy (Caverject, Edex, Tri/Bi-Mix)



Mechanism of action: smooth muscle vasodilator



Administration: 10, 20, 40ug



Inject directly into corporeal bodies of the penis



Results: 70%-90%



Dropout rates: 25%-60%



Side effects: pain (36%), priapism (4%), fibrosis

Androgen Replacement Therapy



Indications: hypogonadism (<285ng/dl)



Avoid oral estrogens-increase LFTs



Injectable – 200mg testosterone (cypionate, enathate, propionate), q2-3 weeks



Transdermal (Patch or gel)



Avoid in patients with prostate or breast cancer



Slight increase risk of BPH



Monitor all patients with annual DRE and PSA

Vacuum Constriction Device

Mechanism of Action:



Penis placed in plastic tube



Air evacuated from the tube



Blood trapped in penis with constricting ring



Erection limited to 30 minutes



Results: 80%-90%



Contraindications: bleeding disorders, sickle cell disease, anticoagulation



Complications: coolness, petechiae, numbness, pain with ejaculation



High drop out rate



Was previously first-line treatment for ED



Seldom used now that oral therapy is available



Considered an alternative if patient fails oral therapy and does not want to proceed
with surgery

Penile Prosthesis

Indications:



Patients who have failed other therapies



Peyronie’s disease



Severe vasculogenic disease

Choosing a Penile Prosthesis

Considerations:



Medical condition



Lifestyle



Cost



Insurance coverage



As with all prescription products, complications are possible

Malleable Prosthesis



Easy for patient and partner to use



Few mechanical parts



Same-day surgery usually possible



Least expensive type of prosthesis

Two-Piece Inflatable Prosthesis



Small inflation pump provides comfort and ease



Fast and easy one-step deflation procedure



Better conceal ability when flaccid than with malleable or self-contained devices

Three-Piece Inflatable Prosthesis



Most closely approximates the feel of a natural erection



Cylinders expand in girth



Some cylinders have the potential to expand in length



When inflated, it feels more firm and more full than other prosthetic erections



When deflated, it feels softer and more flaccid with better conceal ability than with
other prosthetic devices

Penile Prosthesis

Advantages:



Low-morbidity



Low-mortality surgery



Low complication rates



High success rates – 5% malfunction rate at 5 years



High satisfaction rate – 87%



High partner satisfaction rate



Good rigidity



Freedom from medications



Outpatient/24HR surgery



Resume sexual activity 4-6 weeks



No loss of ability to ejaculate or achieve orgasm

Disadvantages:



Surgery



Expensive



Possible mechanical failure

Insurance Reimbursement



Covered by most companies, including Medicare



No co-payment for men with Medicare supplemental insurance

Lec:15

Surgery

MALE INFERTILITY

INFERTILITY

The inability of a sexually active, non-contracepting couple to achieve pregnancy in one year

EPIDEMIOLOGY



25% of couples don’t achieve pregnancy within one year, 15% of them seek medical
treatment.



The chance of normal couples conceiving is estimated to be:

o  20% per month
o  75% by 6 months
o  90% by 1  year



20% of infertility cases are due to male factors & 30-40%of them due to both male &
female factors.



Fertility rates are at their peak in men & women at age 24 years,beyond that age,they
decline in both sexes.



25-35% of infertility couples will conceive at sometime by intercourse alone.

Goals of evaluation of infertile men

1.  Identification of reversible disorders.
2.  Identification of irreversible conditions.
3.  Identification of chromosomal & genetic abnormalities that may affect the offspring.
4.  Identification of idiopathic cases.

Prognostic factors

1.  Duration of infertility.
2.  Primary or secondary infertility.
3.  Results of seminal fluid analysis(SFA).
4.  Age & fertility state of female partner.

Evaluation of infertile male



History.



Physical examination.



SFA.



Adjunctive laboratory investigations.



Radiologic investigations.



Testicular biopsy.

History

Physical examination



Abnormal secondary sexual characters.



Gynecomastia.



Genital examination:



Penis



Scrotum



Spermatic cord.



DRE.

Seminal fluid analysis (SFA)



2 0r 3 samples examined over a period of several weeks for more accuracy.



Sample collection.

Sperm morphology

SFA nomenclature

Adunctive laboratory tests

Semen culture



For pyospermia (3-23% of infertility case).



Immature germ cells vs. leukocytes ??



Indications :
1.  History of genital infection.
2.  Presence of > 1000 pathogenic bacteria/ml.
3.  Presence of >10⁶ WBC/ml.

Semen fructose



Indicated in seminal fluid with low ejaculate volume, acidic PH & no sperms.



Absent in seminal vesicle agenesis or obstruction.

Post ejaculate urinalysis

For suspected retrograde ejaculation.

Hormonal tests



Less than 3% of infertile men have hormonal etiology.



Used to evaluate the hypothalamo-pituitary-gonadal axis.



Testosterone,LH,FSH &prolactin are the main hormones.



Indications of hormonal evaluation:
1.  Sperm density< 10x10^6/ml
2.  Impaired sexual function.
3.  Findings suggestive of a specific endocrinopathy.

Antispermantibody (ASA) test



These antibodies occur if the blood-testis barrier is broken(by testicular trauma or
torsion or by vasectomy).



Indirect Ab. or direct Ab.



Commonly measured by mixed agglutination reaction.



ASA are detected in 10% of infertile men vs. 2% of fertile men.



Indications:
1.  Sperm agglutination or clumping by SFA.
2.  +ve postcoital test(PCT).
3.  Low sperm motility with history of testicular injury or surgery.
4.  Unexplained infertility.

Chromatin/DNA integrity testing.

Electron microscopy



For ultrastructural defects in sperms.



Indicated if sperm motility < 5-10 % with good viability of sperms.

Sperm function tests

1.Sperm-cervical mucus interaction

Indicted in:



Hyperviscous semen.



Low volume semen with normal sperm count.



Suspected cervical mucus abnormalities.



Unexplained infertility.

2.Sperm viability assay (hyposmotic swelling test)

Used if sperm motility<5-10%.

3.Sperm penetration assay

Genetic (chromosomal) tests



Indicated in azospermia or severe
oligospermia.



5.8%of infertile men have genetic defects.



The defects are either:

o Numerical (e.g. klinefilter syndrome).
o Structural (e.g. CFTRG mutations).



The defects are in the sex chromosomes or
autosomes.



Y chromosomes microdeletions ( AZFc is the most common).

Radiologic investigations

Vasography



Used to assess the patency of the vas, seminal vesicles & ejaculatory duct & to aspirate
vasal fluid.



The best timing of it is prior to vasal reconstructive surgery.



Indicated in :

1. Azospermia with normal testicular biopsy.
2. Severe oligospermia

Venography

The best tool to diagnose varicocele & to treat it by embolization (via femoral or internal
iliac veins).

Ultrasonography (US)

1.  Scrotal US: for varicocele or testiculr tumors.
2.  Abdominal US: to detect renal agenesis (in 80% of pt. with unilateral CAVD).
3.  Transrectal U.S.(T.R.U.S.)



To assess the prostate,seminal vesicles,ejaculatory duct &vas.



Indicated in azospermia with suspected ejaculatory duct obstruction.



Equivocal TRUS findings in suspected ejaculatory duct obstruction can be confirmed by
seminal vesicle aspiration.

Testicular biopsy

Either

diagnostic( to differentiate obstructive from non-obstructive azospermia in pt.with normal
testicular size & normal FSH level).

theraputic (to harvest sperms for IVF or for cryopreservation).

Histological forms seen in testis biopsy

1.  Normal testis.
2.  hypospermatogenesis.
3.  Maturation arrest.
4.  Germ cell aplasia(Sertoli cell only syndrome).
5.  End stage testis(sclerotic testis).

Causes of male infertility

varicocele

Abnormally dilated testicular veins within the spermatic cord.

o  Clinical vs. subclinical varicocele.
o  Affects 15%of normal adolescents vs. 20-40% of infertile men.
o  90% left sided-10% bilateral.
o  The most common surgically correctable cause of infertility.

Why it occur?

MULTIFACTORIAL

o  Anatomic variations.
o  Raised Hydrostatic pressure.
o  Raised Testicular temperature.
o  Reflux of renal &adrenal metabolites from renal vein.

ALLreduced testicular size,sperm motility & count  infertility.

 Diagnosed: clinically, SFA, oppler scrotal U.S.

 Treatment

surgical

1.embolization.

2.ligation of dilated testicular veins:

*retroperitoneal

*inguinal

*subinguinal

*laparoscopic

 This Rx. Improve seminal parameters in 70% of pt. & improve conception rate in 40-

50% of couples.

 For whom to do surgery?

 clinical varicocele.

 abnormal SFA or infertility.

 affected testicular growth especially adolescents.

Treatment of male infertility

o  It is better to improve male/female fertility & to allow natural conception
o  If this is not successful, assissted reproductive techniques(ART) are used.
o  Types:



medical Rx.



surgical Rx.



ART.

Medical Rx.

1. Life style modifications.

2. Hormonal Rx.

o Gonadotropins(LH/FSH)

*Used for hypogonadotrophic hypogonadism.

*Formulae: HCG, HMG or recombinent FSH.

o GnRH

uesed only for hypogonadotrophic hypogonadism with intact pituitary function.

o Testosterone Rx.

different formulae are used to induce virilisation in pt. with primary or secondary
testicular failure.

excess testosterone is a male contraceptive.



Antiprolactinaemic drugs For hyperprolactinaemia.



Treatment of thyroid disorders, estrogen excess & corticosteroid excess.



Corticosteroids

*used for immunologic infertility( it accounts for 10% of infertility cases).

*It achieves pregnancy rate = 30-40%.

3. Treatment of pyospermia



proper antibiotics



antioxidants.



frequent ejaculation.

4. Empirical medical Rx.



for idiopathic infertility(25% of *infertility cases).



Not proven effective.



Includes clomiphen citrate, tamoxifen & GnRH/gonadoropins

5. Other drugs

kallikreins,antioxidants,zinc,arginine& L-carnitine.

6. Growth hormones

For oligospermia(under investigations).

Surgical treatment

1. Varicocele Rx.

Ligation of dilated testicular veins to eliminate retrograde reflux of venous blood
via gonadal veins.

Types of surgery:

*percutaneous embolization.

*surgical ligation via:

-retroperitoneal

-inguinal

-subinguinal

-laparoscopic routes.

 Improved seminal parameters in 70% of pt.

 Improved pregnancy rate in 40-50% of pt.

 Complications:

1. recurrence 2. hydrocele

3. vasal injury 4. testicular atrophy.

2. Repair of vasal or epididymal obstruction.

 Vasovasostomy

*indicated for vasectomy reversal.

*Complications

1.testicular atrophy 2. hematoma 3.recurrence(3-12%).

*patency & pregnancy rate:

 Vaso-epididymostomy

 indicated in

reversal of vasectomy for >15 years(if vasovasostomy failed).

epididymal obsruction.

 Patency rate: 30-65%.

 Pregnancy rate: 20-40%.

3. Rx. Of ejaculatory duct obstruction



Ejaculatory duct obsruction accounts for 1-5% of infertility cases.



Treated by transurethral ejaculatory duct resectionn(TUEDR).



Patency rate: 65-70%.



Pregnancy rate: 20-30%.

4. orchidopexy.

5. Surgical Rx. Of pituitary tumors.

6. Rx. Of ejaculatory dysfunction

a. Retrograde ejaculation(RGE)

treated by alfa-agonists or TCA or sperm retrieval for IVF.

b. Anejaculation



absent seminal emission.



mostly caused by spinal cord injury& retroperitoneal lymph nodes dissection &
sometimes psychologic.



Treated by



penile vibratory stimulation or electroejaculation.



The semen obtained is used for IVF.



Success rate: 75%.

7. Rx. Of anatomic,congenital & organic causes of male infertility



Hypospadias repair.



Plication of peyronies disease.



Rx. Of erectile dysfunction.

Assissted reproductive technologies(ART)



Intrauterine insemination(IUI).



In vitro fertilization(IVF).



Intracytoplasmic sperm injection(ICSI).



Gamete intrafallopian transfer(GIFT)

-zygote intrafallopian trasnfer(ZIFT)

-tubal embryo transfer(TET)

Intrauterine insemination

(IUI)

*Indicated in:



male factor infertility.



unexplained infertility.



cervical mucus or anatomic abnormalities that interfere with sperm deposition at the
cervical os.

*Office procedure, no anasthesia.

*Success rate: 15-20%.

*Complications

1.Uterine cramps 2.pelvic infections. 3.Multiple gestations.

IVF



It includes harvesting the oocyte & sperm in order to incubate them for fertilization then
transferring the embryo to the uterine cavity.



Pregnancy rate: 20-30% per cycle.



Costs: 12000-15000 $ per cycle.

Indications:



failed medical or surgical Rx. or IUI.



CBAVD.



severe oligospermia.



cryopreserved sperms.



azospermia( obstructive or non).



few viable sperms in the ejaculate.

Sperms are retrieved for IVF by:

percutaneous epididymal sperm aspiration (PESA)

microsurgical epididymal sperm aspiration (MESA).

Testicular sperm aspiration (TESA).

Testicular sperm extraction (TESE)  microsurgical, nonmicrosurgical

Intracytoplasmic sperm injection(ICSI)



A special micromanipulation of the sperm into the cytoplasm of a harvested oocyte.



Useful in severe oligosprmia,azospermia & ultrasructural sperms defects.



Conception rate: 50% per cycle.

 Varicocele repair,vasovasostomy or vasoepididymostomy are more cost effective

with a better pregnancy rate than IVF/ICSI.

MOST COUPLES PREFER,

NATURAL FOODS,

NATURAL FIBERS,

AND

NATURALLY CONCEIVED BABIES