Benign prostatic hyperplasia by Sayed Eleweedy

Benign Prostatic Hyperplasia
Sayed M Eleweedy
Prof. Of Urology
Urology Department
Alazhar University

Definition
A regional nodular prostatic growth of
varying combination of glandular and stromal
(fibromuscular) proliferation that occurs in
almost men who have testes and who live
long enough
Hyperplasia not hypertrophy

Definition and terminology
• Microscopic BPH
• Histological evidence of cellular proliferation
• Macroscopic BPH
• Organ enlargement due to cellular proliferation
• Clinical BPH
• LUTS thought to be due to BPH

Definition and terminology
BPH (benign prostatic hyperplasia)
– for histological diagnosis only
BPE (benign prostatic enlargement)
– for anatomical diagnosis only
BOO (bladder outlet obstruction)
– for functional diagnosis only
BPO (benign prostatic obstruction)
– functional diagnosis when the prostate is the cause.
LUTS
– Instead of prostatism

Prevalence of pathological BPH with age
48%
29%
11%
92%
87%
77% 31-40
41-50
51-60
61-70
71-80
81+
Age (years)

Prevalence
Clinical BPH develop in 20-50% of men with microscopic or
macroscopic BPH
Clinical BPH in 5-30% of men ages 55-74 years.
Only 40% of them complain of LUTS.
Only 20% of them seek medical advice.

Prostatic Configuration
 LOBAR CONFIGURATION (LOWSLY)
Anterior, Posterior, Middle and 2 Lateral Lobes
 ZONAL CONFIGURATION( McNEAL, 1972, 1968, 1980)
Anterior fibromuscular stroma (30% of the prostatic
volume)
Glandular part (70% of the prostatic volume)
Peripheral zone
Central zone
Transition zone

Prostatic Configuration
Fibromuscular stroma
30% of the prostatic bulk
Has no specific pathology
Peripheral zone
75% of the glandular tissue
Site of cancer
Central zone
– Between peripheral and transition zone
Has no specific pathology
Transition zone
Periurethral zone
Site of BPH

Schematic coronal section of normal prostate

Schematic coronal section of enlarged prostate

Schematic transverse section of normal
prostate

Schematic transverse section of enlarged
prostate
Typical location of benign
nodular hyperplasia.
Posterior displacement
of both peripheral
and central zones.

DHT- a determinant of prostate growth
DHT thought to exert influence over prostate cells via
cascade of molecular interactions
Androgenic action of DHT dependent upon the binding to
the high affinity nuclear androgen receptor (AR) protein
Androgen receptor proteins contain both DHT and DNA
binding domains
Affinity of binding of DHT to AR complex is 5 times higher
than with Testosterone

DHT formation
Testosterone (T) is the
principal androgen
secreted by the testis
T is converted to DHT by
the enzyme 5 a-reductase
(5-AR)
DHT is the active
intracellular androgen that
has the major androgenic
effect
This provides the scientific
basis for the advent of
5-AR inhibitors for the
management of BPH

Type 1 Type 2
Size 259 amino-acids 254 amino acids
Gene location Chromosome 5 Chromosome 2
Enzyme
location
Liver
Non-genital skin
Scalp
Genital tissue
Seminal vesicles
5-alpha reductase enzymes
Occurs as two isoenzymes type 1 and type 2

Growth factors and prostate development
A number of growth factors, expressed by mesenchymal
or epithelial components of the prostate have been identified:
–Stimulatory growth factors :
Epidermal growth factor EGF,
Fibroblast growth factor FGF
Insulin-like growth factor IGF
Transforming growth factor TGF
a
–
Inhibitory growth factors :
Transforming growth factor TGF- b

Growth factors and prostate development
+ Androgen ― Androgen
TGFb1 EGF
bFGF1/FGF2 TGFb1
Apoptosis
Cell Proliferation
Apoptosis
Cell Proliferation
An almost homeostatic relationship between TGFb1 (growth suppressing) and
the Stromal growth promoter bFGF/FGF2
This suggests a degree of resilience to variation in androgen level which may
explain the comparatively slow normal growth of the prostate in response to
continuous exposure to DHT

BPH Development
BPH develops in various stages;
Induction of microscopic hyperplasia
Development of microscopic nodules
Manifestation of clinical BPH :
– Prostatic enlargement
– Bladder outlet obstruction
– LUTS

BPH Development
Microscopic Stromal nodules begin to grow within the prostate around the age of 30 - 40
years
The nodules occur around the transition zone in the Periurethral area and glandular
hyperplasia then develops around them
Nodules vary in size from a few mm to a few cm and contain either:
– Glandular elements
– Fibromuscular elements (Stromal generally the larger component)
– Mixture of both
The nodules will continue to grow in most men when they age

BPH Development
As the amount of glandular tissue grows, the outer layer of prostate tissue
becomes compressed
A tough capsule is created which forces the gland to form lobes
The size and position of the lobes relative to the bladder and urethra can impact
the type and severity of LUTS
If the enlarged prostate encroaches on the urethra obstruction can occur, but this
can also result from an alteration of prostate smooth muscle contractility or
by the prominent median lobe of the prostate behaving as a ball valve

Development of BPH : Intermediate

Normal bladder and prostate
BPH is the most common
neoplasm in man
Pathological changes of this
disorder can be found in 50%
of men in their 5th decade
and in 90% of men in their
ninth decade
The aetiology of BPH is multifactorial
but there are two essential
prerequisites: the presence of
testes and ageing

Pathophysiology
Prostatic hyperplasia increases urethral
resistance, resulting in compensatory
changes in bladder function.

The median lobe projects into the
base of the bladder
The prostatic urethra narrows
The bladder shows trabeculation and
thickening of the wall
Benign prostatic enlargement

Thickening of the bladder wall
Recurrent hematuria
Bladder diverticulum formation
Urinary tract infections
Bladder stone formation
Upper tract dilation
Effects of Benign prostatic obstruction

Renal damage
Renal damage from obstructive
uropathy due to BOO (bladder outlet
obstruction) is a feared complication
It can happen in men with minimal
symptoms and the renal impairment
is not always reversible
The risk of a man with symptoms of
BOO developing renal failure whilst
under follow up is not known for
certain but is minimal

Bladder Changes
Flow is maintained in the early phases of outflow obstruction,
as a result of hypertrophy of the detrusor muscle allows an
increase in detrusor pressure
As outflow obstruction progresses, smooth muscle
hypertrophy occurs followed by connective tissue infiltration
and reduced parasympathetic innervations
Impaired emptying results, caused by decreased compliance
in the bladder wall and secondary detrusor instability, due to
the previous events
Ultimately these changes translate into the persistent
symptoms of frequency, urgency and urge incontinence

Aetiology of BPH – principal hypotheses
The molecular processes underlying the development of BPH
are not completely understood, but androgens and age play a
central role
Several hypotheses have been proposed
– Dihydrotestosterone (DHT) hypothesis
– Oestrogen-testosterone imbalance
– Stromal-epithelial interactions
– Reduced cell death
– Stem cell theory

Aetiology of BPH – Dihydrotestosterone
hypothesis
Adapted from Kirby et al. 199
Dihydrotestosterone (DHT) is the main androgen
responsible for prostate growth.
two isoenzymes of
5-alpha-reductase
have been identified
5-alpha-
reductase
inhibitors
suppress DHT
formation.

BPH Appearance
A characteristic of the gross appearance of BPH are rubbery
yellow/grey nodules of variable size within the prostate
gland
The nodules are composed of epithelium, smooth muscle
and fibrous tissue in varying amounts
Ratio of Stromal tissue to epithelium in BPH varies and has
been suggested to determine the symptomatology of a
BPH patient

Pathologic phase of BPH
Histological changes occur within the prostate but no symptoms
Changes result as a consequence of a neoplastic
transformation of prostatic cells
The prostatic cells begin to behave like embryonic cells,
budding off existing ducts
These later organise to form modules of stroma and
glandular epithelium

Macroscopic phase of BPH
Not all men with histological BPH progress to the
macroscopic phase
The prostate becomes grossly enlarged and symptoms
become apparent in some men
As the amount of glandular tissue grows, the outer layer of
prostate tissue is compressed
This creates a tough capsule that forces the growing gland
to form lobes
The type of severity of symptoms appears to be related to
the size and position of the lobes relative to the bladder
and urethra

Etiologic Theories
Unclear Factors association
Androgens, estrogens, Stromal-epithelial interactions,
growth factors, and neurotransmitters may play a role,
either singly or in combination, in the etiology of the
Multiple factors
– HORMONES
Functioning testes (ANDROGEN INFLUENCE)
DHT Prostate growth, maintenance of size and function
Abnormal accumulation of DHT is the primary cause of BPH
Estrogen/Androgen synergism

Correlated Factors
AGE
TESTES
– Smoking
– Race
– Diet
– Body habitus
– Sexual history
– Vasectomy
– Medications
– Diseases

Etiologic Theories
Stromal-epithelial Interaction Theory
– The stroma may mediate the effect of
androgen on the epithelial components by
production various growth factors

Etiologic Theories
STEM CELL THEORY
– Abnormal maturation and regulation of the cell
renewal process may result into BPH.
– Hormones, growth factors and oncogens may
affect this abnormalities.

Etiologic Theories
Static And Dynamic Components
– STATIC:
Prostatic bulk
Stromal, epithelial and extracellular matrix
– Androgen ablation affect epithelial volume
– Therapeutic modalities to reduce the size of the prostate
– DYNAMIC COMPONENT
Alpha adrenergic receptors
Obstruction by prostatic smooth muscle
– Responsible for variation of symptoms
– Therapeutic modalities that interact with receptors

Stromoglandular hyperplasia of the prostate showing
glandular (upper left) and Stromal (lower right) tissue

Etiologic Theories
Aging, perhaps through vascular mechanisms, leads to further
alteration in bladder biology that in all likelihood amplifies the
effects of obstruction.
Prostate growth is only one component of LUTS in aging men.
Physicians tend to overlook the significant contribution of aging,
bladder dysfunction, nervous system changes, and systemic
disease that in many cases has more impact on symptoms than
the size of the prostate.

Natural history
The natural history of a disease process refers to the
prognosis of the disease over time
BPH Is slowly progressive disease
Spontaneous improvement within(1-5y)
– 18-32% subjective improvement
– 15-32% no change
– 16-60% worsening
– Placebo response 20-40%
– Watchful waiting: 42% improvement
– Placebo/sham studies: 30% improvement

Complications
Bladder stones
UTI
Bladder decompensation
Urinary incontinence
– Overflow
– Detrusor overactivity
Upper urinary tract deterioration and Azotemia
– 0.3-30 % of patients with BPH
Hematuria
– Microvessel density is high in patients with gross hematuria
– Finatstride and treatment of hematuria associated with BPH
Acute urine retention
Mortality

Clinical Picture
Symptoms
Prostatism
LUTS (not symptom specific for BPH)
Irritative
Obstructive

Clinical Picture
Symptoms
OBSTRUCTIVE
– Impairment in the size and force of stream
– Hesitancy
– Intermittency
– Incomplete voiding
– Abdominal straining
– Terminal dribbling

Clinical Picture
Symptoms
IRRITATIVE
– Nocturia
– Daytime frequency
– Urgency
– Urge incontinence
– Dysuria

Clinical Picture
Symptoms
The primary focus of initial evaluation and diagnostic testing is
to establish that the symptoms are, in fact, a result of BPH.
Nonprostatic causes of symptoms can be excluded in a
significant majority of patients on the basis of history, physical
examination, and urinalysis.
Additional diagnostic testing is necessary in patients in whom
the diagnosis is still unclear after initial evaluation

Clinical Picture
Signs
Anatomic Enlargement Of The Prostate
(Examination Or Imaging)

Clinical Picture
Signs
BLADDER CHANGES
– Wall thickening
– Trabeculation
– Diverticular formation
– Calculi
– Chronic distention
– Large residual urine
– Acute retention
– UTI
– Hematuria

Clinical Picture
Signs
Upper Urinary Tract
– Ureterctasis
– Hydroureter
– Hydronephrosis
– Azotemia

Clinical Picture
Signs
Urodynamic Signs
– Decreased Peak flow rate
– Elevated detrusor pressure
– Increase residual urine
– Bladder hyperactivity

Clinical Picture
Signs
Residual Urine
– Measurement
Ultrasonography
Catheter
– 50-100 ml is significant

Clinical Picture
Signs
UROFLOWMETRY
– Least controversy
– Diminished flow
Obstruction
Hypoactive bladder
– Peak flow
<10 ml/sec
>15 ml/sec
10-15 ml/sec

Clinical Picture
Signs
CMG and Pressure Flow Studies
– Filling Cystometry information
Sensation
Compliance
Involuntary bladder contraction
Bladder capacity
– Relationship between flow rate and detrusor
contractility

Differential diagnosis
ImagingLabExaminationPast
history
Symptoms
++
Cystitis
++
Prostatitis
+++Urethral stricture
+++
Prostatic cancer
+++
Neurogenic
bladder
+Bladder stone

Clinical Picture
Initial evaluation
Medical History
– A detailed medical history should be obtained to identify other causes
of voiding dysfunction or co morbidities that may complicate treatment.
– Assessment of LUTS symptom severity and bother
Physical examination
– DRE
– Focused neurological assessment
Urinalysis
Serum creatinine and imaging of UUT
PSA (if life expectancy>10years, if the diagnosis of prostate
cancer can modify the management and before treatment
with 5α-reductase inhibitors)

Symptom Assessment
The International Prostate Symptom Score (IPSS) is
recommended as the symptom scoring instrument
When the IPSS system is used, symptoms classified as:
– Mild (0 to 7)
– Moderate (8 to 19)
– Severe (20 to 35).
IPSS is the ideal instrument to;
– Grade baseline symptom severity
– Assess the response to therapy
– Detect symptom progression in those men managed by
watchful waiting.
IPSS cannot be used to establish the diagnosis of BPH.

Additional Diagnostic Tests
Additional testing should be considered after the initial
evaluation if there is a significant chance the patient’s
LUTS may not be due to BPH.
1. Urinary flowrate
2. Postvoid residual (PVR) urine volume
3. Pressure-flow urodynamic studies
4. Cystourethroscopy
5. Imaging of the UUT:
– Hematuria
– UTI
– Renal insufficiency
– History of Urolithiasis
– History of urinary tract surgery

Evaluation
Men with Symptom score <7
– No absolute or near-absolute indication for treatment
– No further investigation
– WATCHFUL WAITING

Evaluation
Patient with severe symptoms
Candidate for active treatment
– Urodynamic
Flowmetry
Residual urine
– Cystoscopy
Other LUT pathology
Prior to treatment

Voiding time T100 13.5 s
Flow time TQ 12.5 s
Time to max. flow TQmax 4.8 s
Max. flow rate Qmax 18.5 ml/s
Average flow rate Qave 12.2 ml/s
Voided volume Vcomp 158.0 ml
70 year old man
normal flow trace
Uroflowmetry: Unobstructed

Uroflowmetry: Obstructed
Flow time TQ 48.5 s
Average flow rate Qave 2.7 ml/s
Voided volume Vcomp 133.0 ml
70 year old man
moderate obstruction due to BPH
reduced average and peak flow
prolonged duration

:Uroflowmetry Urethral stricture
Flow time TQ 115.0 s
Average flow rate Q ave 4.9 ml/s
Voided volume Vcomp 567 ml
50 year old man
plateau shaped trace
similar Qmax and Qave
long duration

Post-void Residual UrineVol (PVRV)
PVRV measurement is performed non-invasively using Transabdominal U/S
It can be useful in assisting with treatment decisions
It should not be used alone to diagnose BPH
Patients found to have a large PVRV should receive active treatment
Otherwise they may be more likely to develop AUR or fail conservative therapy
Although an increased PVRV may be indicative of obstruction
More than one measurement should be made
Variation has been known to occur between voids
PVRV measurement can also be useful for monitoring:
• improvement or worsening of BPH in non-treated patients

Indication Of Treatment
Absolute Or Near-absolute
 Refractory or repeated retention
 Renal insufficiency
 Recurrent significant hematuria
 Recurrent UTI
 Bladder calculi
 Large residual urine
 Overflow incontinence
 Large bladder diverticulae

Treatment Options
Watchful waiting
Pharmacologic
Mechanical
Endoscopic
Surgical

Treatment Options
Watchful waiting
Reassured that the symptoms are not caused by cancer or
other serious genitourinary pathology, or that the delay in
treatment will not have irreversible consequences
Decreasing total fluid intake especially before bedtime
Moderating the intake of alcohol- and caffeine-containing
products
Maintaining timed voiding schedules.

Treatment Options
Medical treatment
Medical therapy is currently considered the preferred
treatment
Alternative for those individuals who lack absolute
indications for surgery.
– α-adrenergic blockers
– 5α-reductase inhibitors,
– Aromatase inhibitors (decreasing the estrogen)
– Plant extracts.
– Newer therapies:
Antimuscarinic drugs
Phosphodiesterase inhibitors (PDEIs)

Treatment Options
Pharmacologic
Reduce Prostate smooth Muscle tone
– Alpha adrenergic antagonists
Reduce Prostate Bulk
– 5 alpha reductase inhibitors (androgen suppression)
Unknown
– Phytotherapy
– Others

Medical treatment
Alpha blockers:
– Non-selective
– Selective short acting
– Selective long acting (alfuzosin, doxazosin, terazosin)
– Selective alpha 1a blockers (tamsulosin)
5 alpha reductase inhibitors
– Finasteride
– Dutasteride
Combination
Phytotherapy

Treatment Options
Mechanical
Prostatic urethral stent
Balloon dilator
Transurethral thermotherapy
– TUMT
– TUNA
LASER
HIFU

Treatment Options
Endoscopic
Transurethral resection
Transurethral incision
– Electrosurgery
– Laser
– Electrovaporization

Treatment Options
Surgical
Transvesical
Retropubic
Perineal

Minimally Invasive Treatment
For

INTRODUCTION
TURP
• Gold Standard For Decades
• Last Decades Challenges :
• Medical Therapy
• Minimally Invasive Treatments

Minimally Invasive Treatments
 Thermal-based Therapy
 Laser Therapies
 TUVP
 Balloons And Stents
 Chemoablation

Thermal-based Therapy
 Use of high temperature
 Within the prostate
 Coagulative necrosis

Hyperthermia
Temperature < 45
Thermotherapy (TUMT)
Temperature < 45
Low-energy TUMT
High-energy TUMT

Hyperthermia
 Temperature Below 45
 Transurethral
 Transrectal

Hyperthermia
 Temperature < 45
 Microwave
 Randomized Clinical Trials:
 Transient Improvement
 No Proof Of Long Term Efficacy
 Not Recommended By AUA And EUA
 Obsolete

Thermotherapy
LOW-ENERGGY TUMT
 Temperature 45-60
 Short Term Results Good
 Long Term Results Disappointing
 Failure Rate 25-70%
 Abandoned

Thermotherapy
HIGH-ENERGGY TUMT
 Temperature >60
 Short term results good
 Long term results comparable
 Local anesthesia
 Prolonged catheterization (2-4 w)
 At one year retreatment rate 5-15%
 Reserved for
 Patients who prefer to avoid surgery
 Failed medical therapy

Water-induced Thermotherapy(WIT)
• Device consists of:
 Treatment balloon catheter
 18 Fr Catheter Inflatable To 50 Fr
 Heated water circulates within
 Positioning balloon
• Treatment under local anesthesia
• Investigational procedure

High Intensity Focused Ultrasound
Spinal or general anesthesia
Transrectal ultrasound transducer
Temperature of 80-200
Coagulative necrosis
Investigational procedure

Transurethral Needle Ablation(TUNA)
Low radiofrequency energy
 Delivered through catheter equipped with adjustable needles to
selected areas of the prostate
 Producing coagulative necrosis with sparing the mucosa
Temperature 80-100
Local anesthesia
Higher analgesia and sedation
Not recommended as first line treatment

Laser Therapy
Coagulation Necrosis
Tissue Vaporization
Tissue Resection
Tissue Enucleation

Laser Therapy
Visual Laser ablation(VLAP)
Nd YAG
•Nonconduct technique
• Coagulative necrosis
•Conduct technique
• Tissue vaporization
• Tissue resection
• Tissue enucleation
•Advantages
• Less bleeding
• Less TUR syndrome
•Disadvantage
• Prolonged period of catheterization
• No pathological specimen
• Not recommended as first line treatment
• May have a role in high risk patient

Laser Therapy
Interstitial Laser Coagulation
•Cystoscopic control
•Laser fibers directly introduced into the prostate
•Spared mucosa
•Few Irritative symptoms
•Retreatment rate 5-15%
•Not recommended as first line treatment
•May have a role in high risk patient

Laser Therapy
Holmium-laser Resection
Prostatic adenoma is mobilizes
Morcellated
Resected
It is an optional treatment

Transurethral Vaporization of The
Prostate
Modified electrode
Uninterrupted high electrical energy
Vaporization
Disadvantages
Electrode efficacy decreases as tissue desiccate
Electrode must be reactivated

Balloons And Stents
Balloon dilation
Obsolete

Balloons And Stents
Prostatic Stents
Has Significant associated complications
May be indicated only for:
 high risk patients with short life expectancy suffering from urinary
retention

Chemo ablation
• Transurethral injection of absolute alcohol
• Coagulative necrosis
• Investigational treatment

MITs VS TURP
INTRAOPERATIVE COMPLICATIONS
Less bleeding
TUR syndrome free
Offerred for patients with bleeding disorders
Under anticoagulant therapy

MITs VS TURP
POSTOPERATIVECOMPLICATIONS
Significantly higher
Nonablative techniques
Prolonged catheter time
Postoperative dysuria

MITs VS TURP
Sexual Dysfunction
ED Not observed after MITs
Retrograde ejaculation
30% AFTER
TUMT TUNA ILC WIT
>60%
TUVP VLAP HOLR

MITs VS TURP
CLINICAL EFFICACY
There is a close correlation between the degree of
invasiveness and the clinical efficacy
 MODERATE IMPROVEMENT
TUMT TUNA
ILC
 COMPARAPLE IMROVEMENT TO TURP
TUVP HOLR

MITs VS TURP
Durability of response
Rate of secondary intervention
After MITs 14-44%
After TURP 2.6%

MITs VS TURP
ANATOMICAL LIMITATIONS
PROSTATE VOLUME AND SHAPE AFFECT MITs
LARGE PROSTATE IS NOT RELIABLE FOR
VLAP HIFU
TUVP
LARGE MEDIAN LOPE IS NOT A CANDIDATE FOR
TUMT TUNA
HIFU
PROSTATIC CALCIFICATION IS CONTRAINDICATED FOR
HIFU

Surgical Treatment
Of

INTRODUCTION
Absolute indications for prostatectomy
 Refractory urinary retention
 Recurrent urinary tract infection
 Recurrent hematuria refractory to medical treatment
 Renal insufficiency
 Bladder stones

INTRODUCTION
STANDARD SURGICAL TREATMENT
TURP
TUIP
OPEN PROSTATECTOMY

Transurethral Incision Of The
Prostate
Candidate
• Small prostate <20-30 grams
• No middle lobe enlargement

Prostate
Technique
 Electrical knife
 Bladder neck down to the vero
 At 6 oclock
 5 and/ or 7
 Deep incision down to the capsule
 Fat tissue at the bottom

Prostate
Advantages
 Similar improvement to TURP
 In patient with small prostate
 Without middle lobe enlargement
 Fast
 Easy
 Less expensive

Transurethral Resection Of The
Prostate
• Most frequently used method
• Prostate 80-100 grams
• Time limit <60 minutes

Prostate
TECHNIQUE
1. Preliminary cystourethroscopy
Urethral caliber
Unexpected stricture urethra
Other unexpected abnormalities
Identifying landmarks

Prostate
TECHNIQUE
2. Checking resectoscope assembly
• Cutting loop and Coagulation loop and working element
• Position
• Fully backwards withdrawal
• Thickness
• Telescope 30 or 0
• Light source
• Spare lamp
• Light cable
• Screw connection
• Diathermy
• Irrigation
• Tubing connection
• Irrigating fluid

Prostate
TECHNIQUE
3. Passing the resectoscope
 Size of the resectoscope
according to the size of the urethra
 Preliminary OTIS urethrotomy
 Resectoscope sheath with blind obturator
 Resectoscope sheath with visualizing obturator
 Free mobility after insertion

Prostate
TECHNIQUE
4. CUTTING A CHIP
Extending the loop
Levering the shaft of the telescope in the penis
Direct the tip
Depress the loop into the tissue
Continuing cutting with scalloping action
TUR technique for anterior aspect

Transurethral Resection Of
The Prostate
TECHNIQUE
4. CUTTING A CHIP
Tow techniques for cut finishing
 Elevating the beak of the resectoscope before the
cutting loop enters the sheath
 The loop is taken fully inside the sheath
(The beak is not distal to the Vero)

Prostate
TECHNIQUE
4. CUTTING A CHIP
• Length of the ships depends on
• Outside distance of loop from the sheath
• Mobility of the sheath within the urethra

Prostate
TECHNIQUE
4. BLADDER NECK RESECTION
 Trilobar hypertrophy
 Allows floating back of the ships into bladder
 Depth of two cuts is sufficient
 Extra care in case of large middle lobe
Undermining of the bladder neck
Resection of the ureteric orifices
 Hemostasis
 Evacuation of the ships
 Recheck the hemostasis

Prostate
TECHNIQUE
5. LATERAL LOBE RESECTION
 Visibility is clear if not further hemostasis
 Orientation of the landmarks
 Left or right lobe first
 Start at 3 oclock
 Up and down order fashion
 Layer by layer
 Hemostasis for profuse bleeding
 Stoppage at the level of the capsule
 Hemostasis
 Systemic check, 1,3,5 oclock
 Evacuation of the ships

Prostate
TECHNIQUE
6. Tissue In The Roof Of The Prostatic Urethra
Sometimes bulky tissue at the roof
Usually thin and veins are easily breached
Little hypertrophy y in this area
Holding the resectoscope straight to visualize hanging tissue
Better to leave a strip of mucosa at 12 o'clock to reduce incidence
of stricture

Prostate
TECHNIQUE
7. APICAL TISSUE RESECTION
– Require great care
– Incontinence
– Back-cutting is safe
– Clean cut and not to prolong the diathermy
– Hemostasis is short and accurate
– Reduce the thermal injury
– Leave minor bleeding at the apex rather than causing incontinence
– Withdrawing the resectoscope distal to the Veru and held straight to
visualize protruding tissue

The Prostate
TECHNIQUE
7. FINAL HEMOSTASIS
 Systemic hemostasis
 Bladder neck
 mucosal edge
 5 and 7 o'clock
 Lateral lobes
 1, 3, 7, 9, and 11 o'clock
 Apex and either sides of the veru
 Washing out of the remaining ships
 Inspecting diverticulum to remove ships
 Running some irrigant into the bladder before removal of the
instrument

Prostate
TECHNIQUE
8. CATHETERIZATION
 20 or 22 Ch three way
 Check the balloon
300 ml
Completely filled to prevent sliding into fossa
 Catheter introducer
 Check the correct position by irrigation with a syring

The Prostate
PROPLEMS DURING RESECTION
I. PROBLEMS WITH HEMOSTASIS
CAUSES
A. TOO MUCH RESECTION WITH LITTLE ATTENTION
TO HEMOSTASIS AT EACH STAGE
B. TOO DEEP RESECTION WITH VENOU BREACHING
C. RESECTION INSPITE POOR VISIBLITY

The Prostate
Management of profuse bleeding
 Stop resection
 Efforts to stop bleeding
 Warning the anesthetic
 Order blood
 Plasma may be given
 Help if the resectionest is inexperienced

The Prostate
MANAGEMENT OF PROFUSE BLEEDING
 Washing out the bladder
 Attempt to localize the site of bleeding
 Changing into the continuous flow resectoscope
 Chang the electrode to rolley ball type
 Large or atheromatous artery
Compressing the arterial wall
 Opposite side of area of poor visibility
 Venous bleeding coagulation
 Catheter insertion and gentle traction on the bladder neck
 Open surgery

The Prostate
II. PROBLEMS WITH CUTTING
Failure to cut
check the following
 Diathermy unit plugging to the main electric supply
 Diathermy unit switching on
 Foot pedal connection to diathermy
 Correct positioning of the diathermy plate under the patient
 Connection between the diathermy and resectoscope
 Correct irrigant
 Diathermy loop
 Broken
 Properly pushed into the resectoscope ( commonest)
 Thin
 Complete drawing back of the loop during resection without interring cables

The Prostate
III. PROBLEMS WITH POOR VISIBILITY
Check the following
 Bladder fullness
 Light source
 Light cable
 Old with light emerging from its side
 Fully screwed on
 Clean telescope
 Flowing irrigant
 Clear irrigant
 Adequate hemostasis
 Bladder perforation

The Prostate
IV. PROBLEMS WITH CATHETERIZATION
 Catheter introducer
 Recheck the urethra with direct vision
 Ureteric catheter guide the insertion of the catheter

The Prostate
POSTOPERATIVE CARE
IRRIGATION
 Continuous irrigation or forced Diuresis
 Routine set irrigation
 Irrigation for 24-48 hours
 Normal saline
 Speed of irrigation adjustment

The Prostate
POSTOPERATIVE CARE
CONSTIPATION
– Elderly, immobile patient
– Straining causing bleeding
– Adequate hydration
– Mobilization
– Laxatives

The Prostate
POSTOPERATIVE CARE
METORISM
• Abdominal distention with active bowel sounds
• Conservative treatment

The Prostate
POSTOPERATIVE CARE
PATHOLOGY
• Abnormal tissues sent in a separate specimen

The Prostate
POSTOPERATIVE IMMEDIATE
COPLICATIONS
BLOOD LOSS
Bladder lavage
Transfusion
Endoscopic inspection
Open surgery

The Prostate
POSTOPERATIVE IMMEDIATE COPLICATIONS
Catheter Blockage
Blood clots or prostatic ships
Catheter tip syringe suction
Washing out with saline
Catheter change (may be difficult)
Caude catheter or introducer

The Prostate
POSTOPERATIVE COPLICATIONS
CLOT RETENTION
 Restlessness
 Abdominal pain
 Tachycardia
 Low blood pressure
 Distended bladder
 Evacuation of the clots
 Blood replacement
 General anaesthesia may be required

The Prostate
HEMOLYSIS
• Hemolytic irrigant (water)
• Resection time more than three quarters hour
• Intravascular hemolysis
• Water is not used for TURP

The Prostate
SEPTECAEMIA
Prophylactic antibiotic not given
Preexisting unrecognized urinary infection
Rapid pulse
Low blood pressure
Looking ill
No evidence of bleeding

The Prostate
POS-TUR SYNDROME
 Irrigant absorption
 Unrecognized prostatic perforation
 Tachycardia
 Hypertension
 Muscle paralysis
 Confusion
 Local anesthesia rather than general
 Serum sodium
 Diuretics
 Hypertonic saline

The Prostate
POS-TUR SYNDROME
Preventative measures
 Do not use too high pressure during resection
 Use continuous-flow resectoscope
 Saline irrigation postoperatively

The Prostate
POS-TUR HYPEROXALLURIA
 Rare
 Acute renal failure after TURP
 Massive oxalate crystalluria
 Metabolism of absorbed glycine
 Prolonged resection with capsular perforation

The Prostate
POSTOPERATIVE LATER COPLICATIONS
INCONTINENCE
Stress or total
Temporary or perminant
Infection
Bladder instability
Residal obstructing tissue with overflow
Sphincter damage

The Prostate
STRICTURE
 Sites
 Fossa navicularis
 Distal to external sphincter
 Prevention is better than cure
 Use of correct adequate size of resectoscope
 Adequate lubrication
 Otis urethrotomy
 Gentle handling of the instruments

The Prostate
RETENTION
Immediate after catheter removal
Residual tissues
Atonic bladder
External sphincter spasm(Parkinson disease)
Reinsertion of the catheter for couple of days
Recurrent retention do cystourethroscopy
If no residual tissue do urodynamic assessment

Prostate
PREOPERATIVE ADVANCES
Preoperative Use Of Finasteride
 Goal to reduce significant intraoperative bleeding
 3 months preoperatively
 Large prostate (transition zone >30 g)

Prostate
INTRAOPERATIVE ADVANCES
Coagulating Intermitted Cutting Device
 Cutting phase alternating with coagulating phase during each
cut
 Produce efficient coagulation zone with excellent cutting quality
 Decrease bleeding
 Decrease TUR syndrome

Prostate
Transurethral Vaporization
• A modification of TURP
• Thick loop
• Increased electrosurgical settings

Prostate
Transurethral Vaporization
• Comparable results to TURP
• Less bleeding
• Less TUR syndrome
• Shorter period of catheterization
• Longer time of operation

Prostate
Holmium Laser Resection
Advantages
 Shorter catheter time
 Shorter hospital stay
 Reduced risk of bleeding
 Rapid relief of urinary symptoms
Disadvantages
Longer operative time

Prostate
Ethanol-glycine Irrigation
Adverse effect of glycine
 TUR syndrome 2-10%
 Cardiac injury
Adding of 1% ethanol to 1.5% glycine
 Early detection of fluid absorption
 Early detection of ethanol in air
 No adverse effect

Prostate
POSTOPERATIVE ADVANCES
USE OF PELVIC MUSCLE EXERCISES PMEs
PMEs For 15 minutes
3 times daily
4 weeks
Advantages
Early improvement in
Less incontinence
Less frequency
More improvement of quality of life

Prostate
POSTOPERATIVE ADVANCES
Use of bladder infusion prior to trial voiding
• Filling of the bladder before removing the catheter
• Lessens the hospital stay

OPEN PROSTATECTOMY
• Suprapubic Transvesical
• Retropubic

OPEN PROSTATECTOMY
SUPRAPUPIC
• Freyer 1900
• Indications
• Large prostate >80-100 gm
• Large median lobe
• Symptomatic bladder diverticulum
• Large bladder stones
• Obese patient
• Advantage
• Greater visualization of bladder neck and bladder

OPEN PROSTATECTOMY
RETROPUPIC
• Millin 1945
• Indications
• Large prostate >80-100 gm
• Without median lobe
• Thin patients
• Advantages
 Excellent anatomic exposure of the prostate
 Direct visualization of the adenoma during enucleation
 Precise transection of the urethra to preserve urinary continence
 Control bleeding points in the fossa
 Minimal trauma to bladder

In the development of BPH which of the following is
not a growth stimulating factor?
A ) KGF
B ) TGFb
C ) IGF
D ) EGF
E ) bFGF

In the development of BPH which of the following is
not a growth stimulating factor?
A ) KGF
B ) TGFb
C ) IGF
D ) EGF
E ) bFGF
Transforming growth factor beta inhibits epithelial cell
proliferation, the other growth factors stimulate cell division
and differentiation

What is the risk of retention in a 70-79 year old with
moderate lower urinary tract symptoms?
A) 3 per 1000 person years
B )9 per 1000 person years
C )18 per 1000 person years
D )26 per 1000 person years
E )34 per 1000 person years

What is the risk of retention in a 70-79 year old with
moderate lower urinary tract symptoms?
A) 3 per 1000 person years
B )9 per 1000 person years
C )18 per 1000 person years
D )26 per 1000 person years
E )34 per 1000 person years
Data comes from the Olmstead County Study (required
reading) which showed that men aged 70-79 with
moderate/severe symptoms had a retention risk of 34.7 /1000
person years

Regarding the natural history of BPH, what is the
average decline in peak urinary flow rate?
A 0.1mls/sec/year
B 0.2mls/sec/year
C 0.3mls/sec/year
D 0.4mls/sec/year
E 0.5mls/sec/year

Regarding the natural history of BPH, what is the
average decline in peak urinary flow rate?
A 0.1mls/sec/year
B 0.2mls/sec/year
C 0.3mls/sec/year
D 0.4mls/sec/year
E 0.5mls/sec/year
You are required to be aware of the natural history of BPH
and the Olmstead study showed an average decline of
0.2mls/sec/year in patients with BPH

What proportion of men age 61-70 have
pathological evidence of BPH?
A 70%
B 65%
C 60%
D 55%
E 50%

What proportion of men age 61-70 have
pathological evidence of BPH?
A 70%
B 65%
C 60%
D 55%
E 50%
answer:
This figure comes from Barry et al J Urol 1984 which is a
useful paper

What proportion of men aged 50-59 with
BPH have clinical symptoms?
A 15%
B 20%
C 25%
D 30%
E 35%

What proportion of men aged 50-59 with
BPH have clinical symptoms?
A 15%
B 20%
C 25%
D 30%
E 35%
answer:
Garraway et al Lancet 1991 found that 25% of men with a
TRUSS volume of >20mls had an IPSS of >11

What is the most important predictor of
clinical progression in BPH
A Gland size
B Symptom severity
C PSA
D Age
E High post-void residual

What is the most important predictor of
clinical progression in BPH
A Gland size
B Symptom severity
C PSA
D Age
E High post-void residual
A PSA of >1.4ng/ml is the most important predictor of
progression

What is the risk of erectile dysfunction after
TURP?
A 36%
B 30%
C 20%
D 16%
E 6%

What is the risk of erectile dysfunction after
TURP?
A 36%
B 30%
C 20%
D 16%
E 6%
The national prostatectomy audit quotes a rate of 31% however it
appears the risk is much lower. Wasson's TURP vs watchful waiting
study found no difference in the rates of ED between the 2 groups and
Marberger's BJU 1999 meta-analysis indicated a rate of 6.5%

What is the arterial supply of the prostate?
A Superior vesical artery
B Obturator artery
C Inferior vesical artery
D Inferior epigastric artery
E External iliac artery

What is the arterial supply of the prostate?
A Superior vesical artery
B Obturator artery
C Inferior vesical artery
D Inferior epigastric artery
E External iliac artery
The inferior vesical artery supplies the prostate-as it
approaches the gland it divides into urethral and capsular
branches

What are the arteries seen after middle lobe
resection during a TURP?
A Capsular arteries
B Badenoch's arteries
C Floch's arteries
D Branches of the internal pudendal artery
E Branches of the superior vesical artery

What are the arteries seen after middle lobe
resection during a TURP?
A Capsular arteries
B Badenoch's arteries
C Floch's arteries
D Branches of the internal pudendal artery
E Branches of the superior vesical artery
The arteries seen at 5 and 7 o clock after middle lobe resection are
urethral branches of the inferior vesical artery known as Badenoch's
arteries. The smaller arteries seen at 2 and 10 clock are known as
Floch's arteries

What is the embryological origin of the
transition zone?
A Mesoderm
B Ectoderm
C Endoderm
D Mullerian duct
E Mesonephric duct

What is the embryological origin of the
transition zone?
A Mesoderm
B Ectoderm
C Endoderm
D Mullerian duct
E Mesonephric duct
Transition zone arises from mesoderm, peripheral zone
arises from endoderm and central zone appears to be
embryologically distinct possibly mullerian in origin

Which alpha-blocker has the strongest
association with floppy iris syndrome?
A Alfuzosin
B Indoramin
C Prazosin
D Tamsulosin
E Doxasosin

Which alpha-blocker has the strongest
association with floppy iris syndrome?
A Alfuzosin
B Indoramin
C Prazosin
D Tamsulosin
E Doxasosin
Although described as a class effect, the incidence of floppy
iris syndrome with tamsulosin is approx 85%-90%

How much is serum dihydrotestosterone does
reduced by dutasteride?
A 50%
B 60%
C 70%
D 80%
E 90%

How much is serum dihydrotestosterone does
reduced by dutasteride?
A 50%
B 60%
C 70%
D 80%
E 90%
The dual 5ARI reduces serum DHT levels by 90%, the
reduction achieved by finasteride is less but this does not
appear to translate into an increased clinical effect

Which adrenoreceptor subtype mediates
prostatic smooth muscle contraction?
A alpha1-a
B alpha1-b
C alpha2
D alpha1
E alpha1-L

Which adrenoreceptor subtype mediates
prostatic smooth muscle contraction?
A alpha1-a
B alpha1-b
C alpha2
D alpha1
E alpha1-L
The alpha1-a subtype predominates in human stroma and
therefore mediates prostatic smooth muscle contraction

Benign prostatic hyperplasia by Sayed Eleweedy

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