1.
Etiology and Pathophysiology Of
BPH
Dr Ahmed Eliwa
MBBCh, MSc urology
Assistant lecturer in urology and andrology

2.
• What are the factors responsible for prostatic
growth and enlargements
• What's the relation between BPH bladder
obstruction
• What's the bladder response to obstruction
• How can these approach of treatment

3.
• BPH is a pathologic process that contributes
to, but is not the sole cause of, lower urinary
tract symptoms (LUTS) in aging men.
underlying etiology of prostatic growth in older
men, cause-and-effect relationships have not
been established.

4.
• The ideas clinical symptoms of BPH
(prostatism) are simply due to a mass-related
increase in urethral resistance are too
simplistic.
• significant portion of LUTS is due to
age-related detrusor dysfunction and other
conditions such as polyuria, sleep disorders,
and a variety of systemic medical conditions
unrelated to the prostate-bladder unit.

5.
• This has led to the recognition that, although
LUTS commonly may be related to bladder
outlet obstruction (BOO) as a result of benign
prostatic obstruction (BPO), which is often
associated with benign prostatic enlargement
(BPE) resulting from the histologic condition of
BPH, this is not invariably the case.

6.
From Roehrborn CG. Pathology of benign prostatic hyperplasia. Int J
Impot Res 2008;20[Suppl. 3]:S11–8.)

7.
• Failure to empty can be related to an outlet
obstruction or to detrusor under-activity of
the bladder or to a combination of both.
(Reynard et al, 1996).

8.
ETIOLOGY
• Histopathologically BPH is characterized by
an increased number of epithelial and
stromal cells in the periurethral area of the
prostate and thus correctly referred to as
hyperplasia and not hypertrophy
• The precise molecular etiology of this
hyperplastic process is uncertain.

9.
• Androgens
• Estrogens
• Apoptosis
• Stromal-epithelial interactions
• Growth factors
• Neurotransmitters
may play a role, either singly or in combination,
in the etiology of the hyperplastic process.

10.
ROLE OF ANDROGENS

11.
• Although androgens do not cause BPH, the
development of BPH requires the presence of
testicular androgens during prostate
development, puberty, and aging
(McConnell,1995; Marcelli and Cunningham,
1999)

12.
• In the Olmsted County cohort the
estradiol/bioavailable testosterone ratio
increased (Roberts et al, 2004).
• In the prostate the nuclear membrane bound
enzyme steroid 5α-reductase converts the
hormone testosterone into DHT, the principal
androgen in this tissue (McConnell, 1995)

13.
90%
Testicular
10%
Adrenal
Prostatic Androgen

14.
• Inside the cell, both testosterone and DHT
bind to the same high-affinity androgen
receptor protein (Chatterjee, 2003).
• androgen withdrawal leads to the activation
of specific genes involved in programmed cell
death (Kyprianou and Isaacs, 1989;
Martikainen et al, 1990).

15.
ANDROGEN RECEPTORS
• The prostate, unlike other androgen-
dependent organs, maintains its ability to
respond to androgens throughout life.

16.
Two types of steroid 5α-reductase have been
discovered, each encoded by a separate gene
(Russell and Wilson, 1994).
• Type 1 5α-reductase
• Type 2

17.
• Clearly, the type 2 isoform is critical to
normal development of the prostate and
hyperplastic growth later in life.

18.
• ROLE OF ESTROGENS

19.
• experimental BPH, estrogen appears to be
involved in induction of the AR (Moore et al,
1979).
• Estrogen may, in fact, “sensitize” the aging dog
prostate to the effects of androgen (Barrack
and Berry, 1987).
• estrogen treatment stimulates the stroma,
causing an increase in the total amount of
collagen (Berry et al, 1986a, 1986b)

20.
• ER-α is expressed by prostate stromal cells,
and ER-β is expressed by prostate epithelial
cells (Prins et al, 1998).

21.
• From experimental studies with aromatase
inhibitors it appears that decreases in
intraprostatic estrogen in animal models may
lead to reduction in drug-induced stromal
hyperplasia (Farnsworth, 1996, 1999).

22.
REGULATION OF PROGRAMMED CELL
DEATH

23.
• due to epithelial and stromal proliferation or
to impaired programmed cell death leading
to cellular accumulation.
Increased expression of
antiapoptotic pathway genes
(e.g., BCL2) supports this
hypothesis (Kyprianou et al, 1996;
Colombel et al, 1998)

24.
• Androgens not only are required for normal
cell proliferation and differentiation in the
prostate but also actively inhibit cell death
(Isaacs, 1984).

25.
• Neural signaling pathways, especially α-
adrenergic pathways, may also play a role in
balancing cell death and cell proliferation
(Anglin et al, 2002)

26.
• Tenniswood (1992) suggested androgens
providing a modulating influence over the
local production of growth regulatory factors
that varies in different parts of the gland.
• Members of the transforming growth factor-β
(TGF-β) family are likely candidates for this
regulatory step (Martikainen et al, 1990).

27.
STROMAL-EPITHELIAL INTERACTION

28.
• BPH may be due to a defect in a stromal
component that normally inhibits cell
proliferation, resulting in loss of a normal
“braking” mechanism for proliferation.

29.
• The process of new gland formation in the
hyperplastic prostate suggests a
“reawakening” of embryonic processes in
which the underlying prostatic stroma
induces epithelial cell development (McNeal,
1990).
• signaling protein CYR61

30.
GROWTH FACTORS

31.
growth stimulatory factors such as the
• FGF-1
• FGF-2
• FGF-7
• FGF-17 families
• vascular endothelial growth factor (VEGF), and
insulin-like growth factor (IGF) may play a role,
with DHT augmenting or modulating the growth
factor effects.

32.
• FGF-7 is the leading candidate for the factor
mediating the stromal cell–based hormonal
regulation of the prostatic epithelium.
• FGF-7
local ischemia

33.
• A transgenic mouse line Int-2/FGF-3
androgen-sensitive epithelial
hyperplasia in the male mouse
prostate histologically similar to
human and canine BPH (Tutrone
et al, 1993).

34.
OTHER SIGNALING PATHWAYS

35.
• sympathetic pathways may be important in the
pathogenesis of the hyperplastic growth process
(McVary et al, 1994, 2005).
• α-Adrenergic blockade, in some model systems,
can induce apoptosis (Anglin et al, 2002).
• α-Adrenergic pathways can also modulate the
smooth muscle cell phenotype in the prostate
(Lin et al, 2000).

36.
• Renin-angiotensin system (RAS) are present in
prostatic tissue and may be activated in BPH
(Dinh et al, 2001, 2002; Fabiani et al, 2001).
• Either with or without sympathetic
modulation, local RAS pathways may
contribute to cell proliferation and smooth
muscle contraction.

37.
• POTENTIAL ROLE OF
INFLAMMATORY PATHWAYS AND
CYTOKINES IN BENIGN PROSTATIC
HYPERPLASIA

38.
• IL-2, IL-4, IL-7, IL-17, interferon-γ (IFN-γ), and
their relevant receptors are found in BPH
tissue (Kramer et al, 2002; Steiner et al,
2003a, 2003b).
• IL-2, IL-7, and IFN-γ stimulate the proliferation
of prostatic stromal cells in vitro.

39.
• Prostatic epithelial cell senescence results in
increased expression of IL-8, which can
promote proliferation of nonsenescent
epithelial and stromal cells (Castro et al, 2004}

40.
• An excellent recent review of BPH as a
potentially autoimmune disease was
published by Kramer and colleagues (2007),
and illustrates the immunologic key features
of chronic inflammation in BPH and the
present interpretation of these changes in the
development and progression of BPH.

41.
• To date, however, no firm cause-and-effect
relationships have been established between
prostatic inflammation and related cytokine
pathways and stromal-epithelial hyperplasia.

42.
GENETIC AND FAMILIAL FACTORS

43.
• autosomal dominant
• 50% of men undergoing prostatectomy for
BPH when younger than 60 years of age
• 9% of men undergoing prostatectomy for
BPH when older than 60 years

44.
DNA mutations (White et al, 1990)
DNA hypomethylation (Bedford and van Helden, 1987)
abnormalities of nuclear matrix protein expression (Partin et al, 1993)
miscellaneous genetic polymorphisms (Werely et al, 1996;
Konishi et al, 1997; Habuchi et al, 2000)
Abnormal expression of the Wilms tumor gene (WT1)(Dong et
al, 1997)
specific gene or genes involved in
familial BPH or that contribute to the risk
of significant prostatic
enlargement in sporadic disease

45.
PATHOPHYSIOLOGY

46.
Prostatic hyperplasia
increases urethral resistance,
resulting in compensatory changes in
bladder function.
elevated detrusor pressure required to maintain urinary flow in the
presence of increased outflow resistance occurs at the expense of
normal bladder storage function.

47.
Obstruction-induced changes in detrusor
function,
compounded by
age related changes in both bladder and
nervous system function
lead to urinary frequency, urgency, and
nocturia, the most bothersome BPH-related
complaints

48.
• Prostatic smooth muscle represents a
significant volume of the gland (Shapiro et al,
1992)
• Active smooth muscle tone in the human
prostate is regulated by the adrenergic
nervous system (Roehrbornand Schwinn,
2004).

49.
• Receptor binding studies clearly demonstrate
that α1A is the most abundant
adrenoreceptor subtype present in the
human prostate (Lepor et al, 1993a, 1993b;
Price et al, 1993).
• α1A receptor clearly mediates active tension
in human prostatic smooth muscle

50.
• type 4 and type 5 phosphodiesterase
isoenzymes in the prostate and the detrusor
muscle of the bladder implies that
phosphodiesterase inhibitors may be
appropriate candidate therapies for BPH-
related LUTS (Uckert et al, 2001, 2008, 2009).

51.
• kallikrein-kinin system (e.g., bradykinin) may
play a role in the regulation of both smooth
muscle proliferation and contraction in the
prostate (Walden et al, 1999; Srinivasan et al,
2004).

52.
The Bladder’s Response to
Obstruction
• obstruction-induced changes in bladder
function rather than to outflow obstruction
directly.
•
• Approximately one third of men continue to
have significant voiding dysfunction and
mostly storage symptoms after surgical relief
of obstruction (Abrams et al, 1979).

53.
Obstruction-induced changes
detrusor instability or
decreased compliance
are clinically associated
with symptoms of
frequency
urgency.
decreased detrusor
contractility
associated with
deterioration in the force of the
urinary stream,
Hesitancy
Intermittency
increased residual urine
detrusor failure.

54.
smooth muscle hypertrophy
significant intracellular and extracellular changes in the
smooth muscle cell that lead to detrusor instability and
in some cases impaired contractility.
• changes in smooth muscle cell contractile protein
expression,
• impaired energy production (mitochondrial
dysfunction)
• calcium signaling abnormalities
• impaired cell-to-cell communication
increased intravesical pressure and maintained flow
(Levin et al, 1995, 2000).

55.
Skeletal
muscle
hypertrophy
Maintain power
and function
ADAPTIVE
RESPONSE
Detrusor
muscle
change in myosin heavy
chain isoform expression
(Linand McConnell, 1994;
Cher et al, 1996)
significant alteration
in the expression of a variety
of thin filament-associated
proteins (Mannikarottu et al,
2005a, 2005b, 2006).
stress stress
smooth muscle cells revert to a secretory
phenotype in response to obstruction-induced
hypertrophy.
One consequence of this phenotypic switch is
increased ECM production.
The detrusor smooth muscle cell is a key
contributor to the complex of symptoms
associated with prostatic obstruction.
(Christ and Liebert, 2005).

56.
• that obstruction may modulate neural-
detrusor responses as well (Steers et al, 1990,
1999; Clemow et al, 1998, 2000).
• Altered neural control of micturition has been
noted in aging rats, including reduced bladder
contractility, impaired central processing, and
altered sensation (Chai et al, 2000).

57.
INSIGHTS FOR THE TREATMENT

58.
Prostatic
hyperplasia
Prostatic
smooth
muscle
contraction
Detrusor
response
to
obstruction

59.
Prostatic
Hyperplasia
Aromatase
inhibitors

60.
Prostatic
smooth
muscle
contraction

61.
Detrusor
response
to
obstruction

62.
EASY WAY

63.
Terminology
• Benign Prostatic Enlargement
• BPE
• Clinical Dx
• Benign Prostatic Hyperplasia
• BPH
• Pathological Dx
• Bladder Outflow Obstruction
• BOO
• Urodynamic Dx

64.
LUTS and BOO
• 1/3 of men with LUTS do not have BOO
• 5% - 35% of patients with BPH & LUTS do not
improve symptoms after TURP
• LUTS have a poor diagnostic specificity for
BOO
• Prostate size and uroflowmetry have better
correlation with urodynamic study than
symptoms alone

65.
Diagram showing the relationship between histologic hyperplasia of the prostate (BPH), lower urinary tract symptoms (LUTS), benign
prostate enlargement (BPE), and bladder outlet obstruction (BOO). The size of the circles does notrepresent actual proportions but
rather illustrates the partial overlap between the different disease definitions. (From Roehrborn CG. Pathology of benign prostatic
hyperplasia. Int J Impot Res 2008;20[Suppl. 3]:S11–8.)

66.
Prostate Pyramid
Urologist
GP
Lives with symptoms
Asymptomatic

67.
Treatment of BPH
• Treating an enlarged prostate ?
• Treating lower urinary tract symptoms?
• Treating bladder outlet obstruction?
• Can LUTS disappear after treatment?
• Can BOO be relieved after treatment?
• Any complication may occur?
• Is the treatment cost- effective ?

68.
Therapeutic modalities for LUTS
ascribed to the prostate
• Watchful waiting and fluid restriction, natural
history of BPO may wax and wan
• Medical treatment to reduce prostate size or
decrease intraprostatic resistance
• Surgical treatment to remove prostatic
obstruction or reduce urethral resistance
• Minimally invasive therapies

69.
Do I Need an Operation ?
• History (IPSS)ssssssss
• DRE
• U/S Scan - KUB
- TRUS
• Uroflow Test

70.
Minimally Invasive and Endoscopic Management of
Benign Prostatic Hyperplasia
• Intraprostatic Stents
• Transurethral Needle Ablation of the Prostate
• Transurethral Microwave Therapy
• Lasers
• Transurethral Resection of the Prostate
• Transurethral Vaporization of the Prostate
• Transurethral Incision of the Prostate
• Other Technologies

71.
Retropubic and Suprapubic Open Prostatectomy
• Indications for Open Prostatectomy
• Preoperative Evaluation
• Operating Day Preparation
• Surgical Technique
• Postoperative Management
• Complications

72.
• Acute Urinary Retention

73.
Surgery in BPH
Indicated in :
 Severe symptoms and advanced cases
 Acute retention of urine
 Refractory urinary retention
 Persistent hematuria
 Complications like hydronephrosis

74.
Trans-Urethral Resection of Prostate

75.
OTHER TECHNIQUES
 Balloon Dilatation
 Intra Prostatic Stents
 Tuna
 Lasers
 Electro Vaporization
 Vapour Resection

76.
TRANS URETHRAL NEEDLE
ABLATION OF PROSTATE

77.
LASERS
 Holmium
 Green Light PVP
 Diode Laser

78.
• ELECTRO VAPOURIZATION
• VAPOUR RESECTION

79.
Trans Urethral Microwave of
Prostate

80.
How Advancing Technology Change Us !!!

81.
Prostate Resectoscope and TURP

82.
Complications of TUR-Prostate
• Peri-operative bleeding
• Urinary tract infection and urosepsis
• Electrolyte imbalance, hemolysis, acute
tubular necrosis
• Acute pulmonary edema
• Bladder neck or urethral contracture
• Retrograde ejaculation and erectile
dysfunction
• Urge or stress urinary incontinence

83.
Minimally invasive procedure
• Transurethral vaporization- resection of prostate
(TUVRP)
• Ho-YAG laser coagulation of prostate
• Visual laser ablation of prostate (VLAP)
• Transurethral needle ablation (TUNA)
• High intensity focused ultrasound (HIFU)
• Microwave hyperthermia
• Minimally invasive = minimally effective?
• A higher re-treatment rate than TURP although less
complication occurs

84.
Intra-Prostatic Stent

85.
Interstitial Laser Coagulation

86.
Hyperthermia of BPH

87.
Surgical Management
Indications-
• upper tract dilation,
• renal insufficiency secondary to BPH, or
• If the prostate gland is greater than 80 to 100 g,
an open prostatectomy should be performed)
• The standard endoscopic procedure for BPH is a
transurethral resection (TUR) of the prostate
Acute urinary retention
Gross hematuria
Frequent UTI
Vesical stone
BPH related
hydronephrosis or renal
function deterioration

88.
Conventional Surgical Therapy
• Transurethral resection of the prostate (TURP)
• Open simple prostatectomy
106

89.
TURP
• “Gold standard” of surgical treatment for BPH
• 80~90% obstructive symptom improved
• 30% irritative symptom improved
• Low mortality rate 0.2%
107

90.
The “gold standard”- TURP
Benefits
Widely available
Effective
Long lasting
Disadvantages
Greater risk of side effects and
complications
1-4 days hospital stay
1-3 days catheter
4-6 week recovery
108

91.
Complication of TURP
• Immediate complication
bleeding
capsular perforation with fluid extravasation
TUR syndrome
• Late complication
urethral stricture
bladder neck contracture (BNC)
retrograde ejaculation
impotence (5-10%)
incontinence (0.1%)
109

92.
TUR syndrome
• TUR is performed with a non-hemolytic fluid
such as 1.5% glycine (not Saline)
• TUR syndrome may develop from the resulting
hypervolemia and dilutional hyponatremia.
• Patients with TUR syndrome may experience
hypertension, bradycardia, nausea, vomiting,
visual disturbance, mental status changes, and
even seizures.
• Occurs in approximately 2% of patients

93.
Minimally invasive therapy for BPH
• transurethral balloon dilatation of the prostate (TUBDP)
• transurethral incision of the prostate (TUI)
• intraprostatic stent
• transurethral microwave thermotherapy (TUMT)
• transurethral needle ablation of the prostate (TUNA)
• transurethral electrovaporization of the prostate (TUVP)
• photoselective vaporization of the prostate (PVP),
• Cryotherapy
• Transurethral ethanol ablation of the prostate (TEAP),
111

94.
Minimally invasive therapy for BPH
• transurethral laser-induced prostatectomy (TULIP)
• visual laser ablation of the prostate (VLAP)
• contact laser prostatectomy (CLP)
• interstitial laser coagulation of the prostate (ILC)
• holmium:YAG laser resection of the prostate (HoLRP)
• holmium:YAG laser enucleation of the prostate (HoLEP)
• high-intensity focused ultrasound (HIFU) coagulation
• botulinum toxin-A injection of the prostate
112

95.
Destroy prostate tissue with heat
Tissue is left in the body and is expelled over
time (called sloughing)
Transurethral Microwave Therapy (TUMT)
Transurethral Needle Ablation (TUNA®
)
Interstitial Laser Coagulation (ILC)
Water Induced Thermotherapy (WIT)
heat therapies
n
n
n
n
n
n

96.
heat therapies
Benefits
Office treatments
Local anesthesia
Minimally invasive
Reduced risk of
complications as
compared to
invasive surgical
“TURP”
Disadvantages
Some symptoms will
persist for up to 3 months
Cannot predict who will
respond
May require prolonged
catheterization
n
n
n
n
n
n
n

97.
possible side effects of
Urinary Tract Infection
Impotence
Incontinence
heat therapies
n
n
n

98.
surgical treatment

99.
TURP
“Gold Standard” of care for BPH
Uses an electrical “knife” to surgically cut
and remove excess prostate tissue
Effective in relieving symptoms and
restoring urine flow
(transurethral resection of the prostate)
n
n
n

100.
the “gold standard”- TURP
Benefits
Widely available
Effective
Long lasting
Disadvantages
Greater risk of side effects
and complications
1-4 days hospital stay
1-3 days catheter
4-6 week recovery
n
n
n
n
n
n
n

101.
possible side effects of
Impotence
Incontinence
Bleeding
Electrolyte imbalance (TUR Syndrome)
May result in ICU (Intensive Care Unit)
TURP
n
n
n
n
n

102.
TURP : Start

103.
TURP : Middle

104.
TURP : Finish

105.
TURP : Catheter

106.
Side Effects
• Retrograde Ejaculation
• Erectile dysfunction
• TUR syndrome
• Redo rate
• Death
68 %
31 %
5-10%
0.5 %
1 % per year
0.2 %

107.
Conclusions
• B.P.E. is a common condition with many more men suffering symptoms
than present to the medical profession.
• Signs and symptoms vary in their character and severity.
• All patients should have standard assessment in the form of history,
examination and investigations with specialised investigations being
reserved for complicated or equivocal cases.
• Medical and surgical treatment options are available and these should be
discussed with the patient prior to commencement.
• Surgery remains the gold standard in the form of TURP

108.
Principles of Thermotherapy
• Blood supply of BPH adenoma more fragile
than prostate capsule
• Adenoma can be heated to cause necrosis
• Capsule protected by better blood flow
• Tissue necrosis, nerve damage/destruction
lead to improved voiding symptoms

109.
Anatomy of BPH
Normal BPH
Hypertrophied
detrusor muscle
Obstructed
urinary flow
PROSTATE
BLADDER
URETHRA
Roehrborn CG, McConnell JD. In: Walsh PC et al, eds. Campbell’s Urology. 8th ed. Philadelphia, Pa: Saunders; 2002:1297-1336.

110.
Radio Frequency Generator
•Monitors temperature of urethra
and prostate 50 times per second
with Precision Reassurance
Technology
•Computerized graphics allow
physician to view treatment in
real time

111.
Cartridge and Needle Deployment
Disposable Cartridge and
Reusable Handle
Dual Deployment of
Needles and Shields

112.
Schematic of TUNA Procedure
Creation of a Lesion
Completed Procedure
with 8 Lesions

113.
Transurethral Microwave Therapy
• Microwave energy
causes tissue necrosis
• Cooling channels in
catheter cool urethra

114.
Transurethral Microwave Therapy

115.
Interstitial Laser Therapy
• Lesions created
throughout prostate
• Laser fiber alignment
critical
• Median lobe can be
treated

116.
Interstitial Laser Coagulation

117.
Anesthesia Options
• Local (lidocaine jelly)
• Oral narcotics
• Prostate block
• I.V. sedation

118.
Treatment Results After Thermotherapy
• Most patients see improvement in symptoms
• Results not as consistent as TURP
• Bladder function important
• Long term results of TUNA, TUMT and ILT are
similar

119.
TURP (Rotor Rooter)

120.
Transurethral ElectrodesTransurethral Electrodes

121.
The TURP

122.
TURP
“Gold Standard” of care for BPH
Uses an electrical “knife” to surgically cut
and remove excess prostate tissue
Effective in relieving symptoms and
restoring urine flow
(transurethral resection of the prostate)
n
n
n

123.
TURP
• “Gold standard” of surgical treatment for BPH
• 80~90% obstructive symptom improved
• 30% irritative symptom improved
• Low mortality rate 0.2%

124.
The “gold standard”- TURP
Benefits
Widely available
Effective
Long lasting
Disadvantages
Greater risk of side effects
and complications
1-4 days hospital stay
1-3 days catheter
4-6 week recovery
n
n
n
n
n
n
n

125.
Laser Prostatectomy
1. PVP
2. Thulium
3. Diode

126.
Minimally invasive therapy for BPH
 transurethral laser-induced prostatectomy (TULIP)
 visual laser ablation of the prostate (VLAP)
 contact laser prostatectomy (CLP)
 interstitial laser coagulation of the prostate (ILC)
 holmium:YAG laser resection of the prostate (HoLRP)
 holmium:YAG laser enucleation of the prostate
(HoLEP)
 high-intensity focused ultrasound (HIFU) coagulation
 botulinum toxin-A injection of the prostate

127.
Laser Wavelengths

128.
ABSORPTION vs. WAVELENGTH
980nm is 2300 times more absorbed in H2O than 532nm
532nm is 74 times more absorbed in HbO2 than 980nm
200W
120W
70W

129.
Optical Penetration Depth
KTP
532 nm
Diode
830 nm
Nd:YAG
1064 nm
Ho:YAG
2100 nm
CO2
10 m
Tissue
0.8 mm
5 mm
10 mm
0.4 mm 0.02 mm
Diode 980nm RevoLix

130.
Laser ablation - VLAP
• Visual laser ablation of the prostate
• Side-firing laser – Nd:YAG
• Non-contact technique
• Large volume tissue coagulation
• Coaguative necrosis with delayed
healing, with tissue slough
• Contact technique – vaporisation
• LA + iv sedation

131.
ILC-Intersitial laser coagulation
• Creation of intraprostatic
coagulative by laser light at
low power
• Cystoscopy + direct
introduction of laser
through urethral mucosa
• Diode laser

132.
Holmium laser prostatectomy
• Ho:YAG: excellent for
incisional prostectomy
• HoLEP: Retrograde
enucleation of prostate
• HoLRP: Retrograde excision
of hyper plastic tissue
• Relatively slow procedure
with a steep learning curve

133.
PVP Laser Prostatectomy
• Vaporizes tissue
• Minimal bleeding
• No catheter post-op

134.
Uses a very high powered green laser and a thin,
flexible fiber
Fiber is inserted into
the urethra through a
cystoscope
How does PVP work?
n
n

135.
Quickly and precisely vaporizes and
removes the enlarged prostate tissue
The green laser energy is hemostatic, so
there is almost no bleeding
How does PVP work?
n
n

136.
Pre Op Immediate Post Op
3 Months Post Op

137.
PVP Laser Removes Tissue
• Opens bladder neck
• Cavity similar to TURP
• Improvement in symptoms similar
to TURP
• Less impotence than TURP, other
morbidity similar

138.
Mean Peak Flow Rate (ml/s)
7.8
27.3 26.2
23.3 23.4
0
5
10
15
20
25
30
pre-op 1 year 2 years 3 years 5 years
pre-op
1 year
2 years
3 years
5 years
Malek et al., Mayo Clinic, Durability Study
Green Light PVP

139.
Post Void Residual (ml.)
154
44 38
51
21 26
0
20
40
60
80
100
120
140
160
Pre-op 3 mos 6 mos 12 mos 24 mos 36 mos
post-v
Malek et al., Mayo Clinic, Durability Study
Green Light PVP

140.
AUA Semptom Skoru
22.0
3.9 3.6 3.6 2.9
0.0
5.0
10.0
15.0
20.0
25.0
pre-op 1 year 2 years 3 years 5 years
AUA symptom
score
Malek et al., Mayo Clinic, Durability Study
Green Light PVP