2. DEFINITION
• Priapism is a full or partial erection that
continues more than 4 hours beyond sexual
stimulation and orgasm or is unrelated to
sexual stimulation
3. HISTORICAL PERSPECTIVES
• The term priapism has its
origin in reference to the
Greek god Priapus, who
was worshipped as a god
of fertility and protector of
horticulture.
• This painting depicts
Priapus weighing his
phallus against a large bag
of coins.
4. • The first recorded account of priapism in English
medical literature is attributed to Tripe(1845).
• Frank Hinman described the natural history of priapism
(Hinman, 1914).
• He first described “acute transitory attacks of priapism”
as opposed to persistence or rapid recurrence of a
single episode.
• Subsequently in 1960 his son Frank Hinman Jr.
proposed that venous stasis, increased blood viscosity,
and ischemia were responsible for priapism and
emphasized that failure to correct these abnormalities
in the penile environment was essentially responsible
for treatment nonresponse (Hinman, 1960)
6. • The penis is composed of 3 corporeal bodies:
• 2 corpora cavernosa and 1 corpus spongiosum.
• Erection is the result of smooth-muscle relaxation
and increased arterial flow into the corpora
cavernosa, causing engorgement and rigidity.
• Corporeal relaxation causes external pressure on
the emissary veins exiting the tunica albuginea,
trapping blood in the penis and causing erection.
7. • Engorgement of the corpora cavernosa
compresses the venous outflow tracts (ie,
subtunical venules), trapping blood within
the corpora cavernosa. The major
neurotransmitter that controls erection is
nitric oxide, which is secreted by the
endothelium that lines the corpora
cavernosa.
11. Pathophysiology of priapism
• These events occur in both normal and
pathologic erections.
• The pathophysiology of priapism involves
failure of detumescence and is the result of
the underregulation of arterial inflow (ie, high
flow) or, more commonly, the failure of
venous outflow (ie, low flow).
• Priapism typically involves engorgement of
corpora cavernosa.
• The corpus spongiosum is typically not
engorged.
12. • Prolonged low-flow priapism leads to a painful
ischemic state,
• which can cause fibrosis of the corporeal smooth
muscle and cavernosal artery thrombosis.
• The degree of ischemia is a function of the
number of emissary veins and the duration of
occlusion.
• Light-microscopy studies conducted early on
demonstrated that corporeal tissue becomes
thickened, edematous, and fibrotic after days of
priapism.
13. Epidemiology
• The frequency of priapism depends on the
population being considered.
• The combination of intracavernosal agents
and other drugs is the cause of approximately
21-80% of all adult priapism.
• Agents used to treat erectile dysfunction are
common causes of adult priapism in the
Western world.
• The overall rate of priapism in persons using
these agents ranges from 0.05-6%.
14. • At other centers, sickle cell disease (SCD)
and sickle cell trait predominate as the cause
of adult priapism. The rate of priapism in
adults with SCD is as high as 89%.
• Approximately two thirds of all pediatric
patients who have priapism also have SCD.
• The rate of priapism among children with
SCD is as high as 27%.
15. • Race
• Priapism is common in African Americans
with SCD.
• Age
• Priapism can occur in males of any age
group, with peaks at age 5-10 years and
20-50 years.
• Among patients with SCD, the prevalence
is higher in men aged 19-21 years.
16. Morbidity
• Priapism is painful at onset. Corporeal fibrosis due to
persistent priapism can result in deep-tissue infections
of the penis.
• The major chronic morbidity associated with all types
of priapism is persistent erectile dysfunction and
impotence.
• The duration of symptoms is the most important factor
affecting outcome.
• A recent Scandinavian study reported that 92% of
patients with priapism for less than 24 hours remained
potent, while only 22% of patients with priapism that
lasted longer than 7 days remained potent.[2]
19. Definitions
• Ischemic priapism (low-flow) is a persistent erection
marked by rigidity of the corpora cavernosa, with little
or no cavernous arterial infow.
• Nonischemic priapism (arterial, high-flow) is a
persistent erection caused by unregulated cavernous
arterial infow. The corpora are tumescent but not rigid,
and the erection is not painful.
• Stuttering priapism describes a pattern of recurrence.
The term has traditionally described recurrent
prolonged and painful erections in men with SCD.
22. • Brazilian banana spider,
Phoneutria nigriventer,
• The venom contains a
neurotoxin that has
calcium channel blocking
properties, inhibits
glutamate release, and
inhibits calcium reuptake
and glutamate reuptake.
• Bites can cause intense
pain, loss of muscle
control—paralysis,
breathing problems—
asphyxiation, and
priapism
24. Ischemic Priapism
(Veno-Occlusive, Low-Flow)
• It is a persistent erection with little or no cavernous
arterial inflow.
• In IP - progressive hypoxia, hypercarbia, and acidosis.
• The patient typically C/O penile pain after 6 - 8 hrs.
• The condition is analogous to a muscle compartment
syndrome, with initial occlusion of venous outfow
and subsequent cessation of arterial infows.
25. Etiopathogenesis of Ischemic Priapism
• It is the most common form of priapism and also the
most serious and dangerous because of the acute
ischemia of the corpora cavernosa.
• The seriousness is directly related to severity of the
obstruction and the duration of the blockage of the
corpora cavernosa.
• Cavernous hypoxia and acidosis begin after 4 hours
and increase to peak levels in 24 hours.
• PO2 and pH of the trapped blood decrease to the
levels of anoxia and acidosis.
26. • Hypoxia and acidosis lead to loss of
contractility of the cavernous smooth muscle,
impairing the venous stasis.
• Histological changes start with edema of the
cavernous tissue, then anoxia and necrosis of
the cavernous smooth muscle cells, leading to
irreversible fibrosis and may be replaced by
collagen, which will result in ED.
• TGF-β may be involved in the progression of
the corporal smooth muscle to fibrosis.
27. Sickle Cell Disease
• SCD priapism has traditionally been ascribed to
stagnation of blood within the sinusoids of the
corpora cavernosa during physiologic erection,
secondary to obstruction of venous outflow by
sickled erythrocytes
• Hemolysis releases hemoglobin into the plasma.
28. Sickled erythrocytes release arginase-I into blood plasma, which converts
L-arginine into ornithine, effectively removing substrate for NO synthesis.
Free Hbg reacts with NO to produce methemoglobin and nitrate.
This is a scavenging reaction; NO is oxidized to inert nitrate.
29. • The combined effects of NO scavenging and
arginine catabolism result in a state of NO
resistance and insufficiency termed
hemolysis-associated endothelial dysfunction
• Hemolysis and reduced nitric oxide are
responsible for the pathogenesis of leg ulcers,
priapism, and stroke in SCD patients.
30. Iatrogenic Priapism: Intracavernous Inj
• Intracavernous Inj may result in low-flow
priapism.
• Most common drugs are papaverine, PGE1,
phentolamine, and moxisylate.
• In most of these cases, priapism result from an
over dosage of these drugs.
• The incidence of priapism is less with PGE1 or
combinations than papaverine alone.
– PGE1 – 1%
– Papaverine – 33%
31. Etiology of Stuttering Priapism
• The term has been used to describe recurrent
unwanted and painful erections in men with SCD.
• Patients typically awaken with an erection that
persists up to 4 hours and becomes progressively
painful secondary to ischemia.
• SCD patients may experience stuttering priapism
from childhood.
• Patients experience repeated painful intermittent
attacks up to several hours before remission.
32. Molecular Basis Of Ischemic And
Stuttering Priapism
Imbalance of vasoconstrictive and vasorelaxatory mechanisms
hypoxia and acidosis of penis
Impairment corporal smooth muscle contractility
and significant apoptosis of smooth muscle cells
Fibrosis of the corpora cavernosa
33. • Ischemia – upregulation of hypoxia-induced
growth factors.
• TGF-β is a cytokine that is vital to tissue repair.
• It is hypothesized that TGF-β may be involved
in the progression of the corporal smooth
muscle to fibrosis.
34. vascular endothelium
vaso-constrictor factors -
RhoA/Rho-kinase
vaso-relaxing factors -
NO and adenosine
priapism-related destruction of the vascular endothelium
cGMP production in low steady-state amounts
alter cGMP dependent feedback control mechanisms
Downregulation of the set point of PDE5 function
35. erectogenic stimulus –
neuronal production of NO
↑↑↑ cGMP
Insufficient PDE5 enzyme to
degrade cGMP
Excessive smooth muscle
relaxation
reduced Rho-kinase activity
diminished smooth muscle
contraction
ISCHEMIC PRIAPISM
36. Pathophysiology of Nonischemic
(Arterial, High-Flow) Priapism
• Non-ischemic priapism is much rarer than ischemic
priapism
• The etiology is largely attributed to trauma
– straddle injury to the crura
– Coital trauma,
– kicks to the penis or perineum,
– pelvic fractures,
– birth canal trauma to the newborn male,
– needle lacerations,
– complications of penile diagnostics, and
– vascular erosions complicating metastatic infiltration of corpora
37. • Iatrogenic injury:
– cold-knife urethrotomy,
– Nesbitt corporoplasty, and
– deep dorsal vein arterialization
• Laceration of cavernous artery can produce unregulated
pooling of blood in sinusoidal space
• Sustained partial erection may develop 24 hours
following trauma.
• Nocturnal erection disrupts the clot and the damaged
artery ruptures and the unregulated arterial inflow
creates a sinsusoidal fistula.
• As healing progresses the fistula forms a pseudocapsule.
• Formation of a pseudocapsule may take several weeks
to months.
38. • The cavernous environment does not become ischemic
and does not require emergent intervention
• Unlike the situation in low-flow priapism, there is no
transformation of the trabecular smooth muscles into
fibroblasts even after prolonged periods, and therefore
these patients are unlikely to develop ED as a direct
consequence of the priapism
• Tissue is well oxygenated and there is the lack of ischemia
and necrosis; so patients rarely complain of pain.
39. PATHOLOGY
• Penile tissue necrosis and progressive fibrosis
are the end-stage manifestations of ischemic
priapism, hampering the physical reactivity of the
erectile tissue and its elasticity needed for
physiologic blood engorgement.
• After 12 hours, Trabecular interstitial edema
develops;
• After 24 hours, the sinusoidal endothelium is
denuded and thrombocytes adhere to the exposed
basement membrane; and
• After 48 hours, thrombi form in the sinusoidal
spaces and smooth muscle cells undergo necrosis or
become transformed to fibroblast-like cells
40. • Irreversible effects resulted most
consistently from the combination of
hypoxia, acidosis, and glucopenia at a time
interval of 4 hours
• Pathologic changes also occur in the penis
when ischemic priapism is relieved. In this
event, as a result of reperfusion injury, the
cavernosal tissue sustains damage from
oxidative stress.
42. History
• Duration of erection
• Presence of pain
• Previous episodes of priapism and method of treatment
• Baseline erectile function
• Use of any erectogenic therapies
• Medications and recreational drugs
• Sickle cell disease, hemoglobinopathies,
hypercoagulable states
• Trauma to the pelvis, perineum, or penis
43. • History of malignancy (prostate cancer)
• Penile prosthesis: The permanent erection
that occurs with some penile prostheses may
mimic priapism.
• Recent urologic surgery
44. Physical examination
• It reveals the rigidity of the
penis, which will help in the
D/D of low-flow and high-
flow priapism.
• Low-flow priapism causes
rigid erections but a normal
corpus spongiosum keeping
the glans penis soft.
• Tenderness, severe pain
(especially after four hours)
and loss of elasticity of the
penis also helps to identify
low-flow priapism.
45. Other Aspects of the physical
examination are as follows:
– Penile color, rigidity, and sensation (soft glans
vs firm glans)
– Penile discharge, lesions, or both
– Evidence of local trauma
– Presence of prosthetic devices: Hardware
malfunction may cause pseudopriapism.
– Regional lymphadenopathy (ie, metastatic
disease)
– Rectal tone: High spinal cord lesions or
stenosis may cause priapism.
46. • Although malignancies rarely cause priapism,
examination of the abdomen, testicles, perineum,
rectum, and prostate may help identify a cancer primary.
• Malignant infiltration of the penis can cause indurated
nodules within corporal tissue.
• Aspiration of cavernosal blood
may act as both diagnostic
and therapeutic maneuver.
48. • Blood gas testing and color duplex
ultrasonography are currently the most
reliable diagnostic methods of distinguishing
ischemic from nonischemic priapism .
• Blood aspirated from the corpus cavernosum
– in pts with ischemic priapism is hypoxic and
therefore dark, “crankcase oil” appearance
– while in pts with nonischemic priapism is normally
oxygenated and therefore bright red.
49. Initial corporal aspirate in ischemic priapism show dark, deoxygenated
blood. Subsequent aspirations will show brighter blood
50. • - Aspiration of penile blood and analysis
• - Duplex ultrasonography
Ph PO2 Pco2
ischemic <7.25 <30 >60
Non ischemic >7.3 >50 <40
51. Color Doppler ultrasonography
• It should be performed in the
lithotomy or frog leg
position, scanning in the
perineum first and then
along the entire shaft of the
penis.
• USG can be used as an
alternative to blood gas
sampling to differentiate
ischemic from nonischemic
priapism
52. • Scanning of the penis should be performed
before aspiration in ischaemic priapism.
• Examination of the penile shaft and perineum
is recommended. In ischaemic priapism there
will be an absence of blood flow in the
cavernous arteries.
• The return of the cavernous artery waveform
will result in successful detumescence.
53. • ischemic priapism ---- no blood flow in the
cavernosal arteries,
• nonischemic priapism ----- normal to high blood
flow velocities in the cavernosal arteries.
• As a screening test for anatomical abnormalities,
such as a cavernous artery fistula or
pseudoaneurysm, in men who already have the
diagnosis of nonischemic priapism.
54. Doppler image of arterial sinusoidal fistula
of left cavernous artery
55. • Penile arteriography may be used as an
adjunctive study to identify the presence and
site of a cavernous artery fistula (ruptured
helicine artery).
• Penile arteriography should be reserved for
the management of high-flow priapism,
when embolization is planned
56. MRI
Three possible roles in the
assessment of priapism
1. imaging of a well-established
arteriolar-sinusoidal fistula
2. to demonstrate the presence
and extent of tissue thrombus
and corporal smooth muscle
infarction.
3. imaging of corporal metastasis
mimicking priapism or causing
true ischemic priapism by
obstruction of venous outflow.
57.
58. Saggital MRI of the penis showing
metastatic deposits of prostate cancer
to the corpus cavernosum
Coronal MRI of the same patient
showing proximal and distal metastic
deposits of prostate cancer
60. Laboratory Testing
• Hb,
• WBC with blood cell differential,
• platelet count,
• coagulation profile
• reticulocyte count and hemoglobin electrophoresis
should be considered in all men unless there is
another obvious cause of priapism
• Emergency setting - screening for SCD should be
performed by either the Sickledex test or
examination of a peripheral smear
61. Sickledex test
• Deoxygenated Hb-S is insoluble in the presence of a
concentrated phosphate buffer solution and forms a
turbid suspension
• A POSITIVE test - cloudy, turbid suspension through
which the black lines are NOT VISIBLE.
• A NEGATIVE test - transparent suspension through
which the black lines are CLEARLY VISIBLE
62. Limitations of Sickledex test
• False positives - erythrocytosis, hyperglobulinemia,
extreme leukocytosis or hyperlipidemia
• False negatives - in infants under six months of age
due to elevated levels of Hemoglobin F
• False positives or false negatives - in pts with a
recent blood transfusion or pts with severe anaemia
63.
64. Management of Ischemic priapism
• Therapeutic goals are to
– alleviate pain and fear,
– abort the erection,
– maintain detumescence and
– prevent long-term complications, particularly ED.
• Management of ischemic priapism must proceed
in a stepwise fashion depending upon the degree
of response to each intervention.
65. • The recommended initial treatment of ischemic
priapism is the decompression of the corpora
cavernosa by aspiration.
• Aspiration alone may relieve priapism in 36% of pts.
• Aspiration should be repeated until fresh bright red
blood is obtained.
• This process leads to a marked decrease in the
intracavernous pressure, relieves pain, and
removes anoxic, acidotic, and hypercarbic blood
66.
67. • A large-bore, 19-21gauge needle should be inserted at
the peno-scrotal junction at 2 o’clock or 10 o’clock
positions.
• The surgeon should compress the penile shaft just below
the 19-gauge needle, aspirating the shaft until it is soft.
• The shaft is permitted to refill. Compression is reapplied
and aspiration repeated
71. • Phenylephrine – agent of choice
(selective α1-adrenergic agonist
without β-mediated ionotropic and
chronotropic cardiac effects)
• phenylephrine can be concentrated
as 200 μg/mL in normal saline and
administered intermittently as 0.5
mL to 1.0 mL, every 5 to 10 mins
• Other Sympathomimetic drugs
(phenylephrine, ephedrine,
epinephrine, norepinephrine)
72. side effects of intracavernous sympathomimetics
– headache,
– dizziness,
– hypertension,
– reflex bradycardia,
– tachycardia, and
– irregular cardiac rhythms
73.
74. Treatment of SCD-induced
ischemic priapism
– analgesics,
– hydration,
– oxygen,
– bicarbonate,
– blood transfusion.
• systemic therapy alone is not effective
management of SCD priapism
• best resolution rates are achieved with therapies
directed at the penis
75. Treatment of Stuttering Priapism
• Goal of the management is prevention of future
episodes
• Oral α adrenergic medications (e.g., etilefrine 0.5
mg/kg/day at bedtime)
• Harmonal therapy - GnRH agonists, antiandrogens
– contraindicated in
• children who have not completed their growth and
sexual maturation
• those trying to conceive
76. • Baclofen - oral 40 mg at bedtime
– Inhibits penile erection and ejaculation, through GABA
receptor activity
• PDE5 inhibitors - selective vasodilation of the
corporal blood vessels prevents sickling of red cells
in the corporal bodies
– Sildenafil - 25 mg oral daily
– Tadalafil - 5 or 10 mg three times weekly
• Intracavernosal self-injection of phenylephrine
should be considered in patients who either fail or
reject systemic treatment of stuttering priapism
77. • Oral terbutaline a beta-2-agonist with minor
beta-1 effects and some alpha-agonist activity.
• A dose of 5 mg has been suggested to treat
prolonged erections lasting more than 2.5
hours, after intracavernosal injection of
vasoactive agents, although the mechanism of
action is not yet fully understood.
• Its main use is in the prevention of recurrent
episodes of prolonged erection.
78. Surgical Treatment of Ischemic
Priapism
• A surgical shunt should not be considered as
first-line therapy
• Surgical treatment is considered only after
– a trial of intracavernous injection of
sympathomimetics has failed or
– if such an attempt has resulted in a significant
cardiovascular side effect
79. Shunts….
• Principle of shunt procedures is to reestablish
corporal inflow by relieving venous outflow
obstruction;
• this requires creation of a fistula between
– the corpora cavernosa (CC) and glans penis,
– CC and corpus sponsigosum, or
– CC and dorsal/ saphenous veins
80. Shunts….
• Percutaneous distal shunts—Ebbehoj (1974),
Winter(1976), or T-shunt (Brant, 2009)
• Open distal shunt—Al-Ghorab (Hanafy, 1976; Borrelli,
1983) or Corporal Snake (Burnett, 2009)
• Open proximal shunt—Quackles (1964) or Sacher (1972)
• Saphenous vein—Grayhack (1964)
• Deep dorsal vein shunt—Barry (1976)
81. Shunts….
• A cavernoglanular (corporoglanular) shunt
should be the first choice of the shunting
procedures because it is the easiest to
perform and has the fewest complications.
• Proximal shunting may be warranted if more
distal shunting procedures have failed to
relieve the priapism.
82. Winter shunt
• A large-bore needle or
angiocatheter is placed in
the distal glans and corpus
cavernosum.
66 % resolution rateCan be performed in ER, in theory
83. Ebbehoj shunt
• A glans-cavernosal shunt is
made with a No. 11 blade.
• Intracavernosal pressure is
monitored.
• After skin closure,
maintenance of pressure at
40 mmHg or less for 10 min
or more is indicative of an
adequate shunt
73 % resolution rate
Penile anesthetic block
84. T-shaped shunt
• T-shaped glans-cavernosal
shunt using a No.10 scalpel.
• The blade is inserted into
each corpus cavernosum
from the glans, turned 90
degrees laterally and then
pulled out to create a T-
shaped shunt
Penile anesthetic block
85.
86. • Note the differences
between the Ebbehoj
and T shunts
87. Open-Al Ghorab
• An open corporoglanular shunt is indicated if
percutaneous shunting fails to reestablish
cavernous blood inflow.
• In this the excision of circular cone segments
of the distal tunica albuginea (5 × 5 mm) is
performed.
88. The transverse incision is made on
the dorsal aspect of the glans 1 cm
distal to the coronal sulcus and
dissection is carried down to the
bulging corporal bodies
A wedge of tunica is excised.
The penis is made flaccid by manual
compression and release.
The skin is sutured with chromic
suture.
74 % resolution rate
89. Open Distal Shunts- Corporal
“Snake” Maneuver
• Modified Al-Ghorab Shunt
• Under GA, a 2-cm transverse incision is
made on the glans;
• The distal tips of the rigid CC are incised
and grasped with Kocher clamps.
• Deoxygenated blood is milked out,
• 7/8 Hegar dilator is advanced through the
tunica to release blood and thrombus
90. Proximal shunts
• If distal shunting fails, then proximal shunting is
recommended.
• Proximal shunting establishes a communication
between the corpora cavernosa and spongiosum at
the base of the penis.
• Shunting may also be accomplished with vein grafting
to the corpora cavernosa.
• Venous shunts have increased the risk of
thromboembolism.
91. Quackels Cavernoso-Spongiosal Shunt
The shunt is created in the perineum between the urethral
bulb and crura. If placed too distal, it will not be effective and will
carry a higher risk of urethral injury
77 % resolution rate
92. Sacher Cavernoso-Spongiosal Shunt
• Bilateral shunts are
created between the
urethral bulb and crura
• The right and left sides
are separated by a
distance of at least 1 cm
in an effort to minimize
the risk of urethral
stricture
93. Barry Cavernoso-Dorsal Vein Shunt
• The deep dorsal vein is
anastomosed to the
tunica albuginea.
• A wedge of tunica
tissue is excised that is
proportionate to the
size of the dorsal vein.
94. Grayhack Cavernoso-Saphenous Shunt
• The saphenous vein is
mobilized by dividing
and ligating the
tributaries.
• The saphenous vein is
spatulated and
anastomosed to the
tunica
• High rates of
thrombosis and PE
76 % resolution rate
95. Assessing Shunt Patency
• Visualization of bright red blood in corporal aspirate
• Corporal blood gas
• Color Doppler ultrasound
• Measurement of intracavernous pressure
• Penile compression maneuver (squeeze and release)
96. Complications of shunts
• penile edema,
• hematoma,
• infection
• Higher rates of ED with proximal shunts
• thrombosis and PE (venous shunts)
• urethral fistulae
• purulent cavernositis
97. Immediate Implantation of Penile
Prosthesis
• penile prosthesis should be considered if:
– The patient has failed aspiration and sympathomimetic intracavernous
injection.
– The patient has failed distal and proximal shunting.
– Ischemia has been present for longer than 36 hours
• Advantages:
– No corporal fibrosis
– penile length may be preserved
• Irreversible
• higher rates of complications:
– infection, urethral injury, device migration, device erosion, and revision
surgeries
98. Ischemic Priapism- Outcomes
• The longer the episode, the less likely for preservation of
erectile function
• Pryor (1982)- > 24h = > 90% ED rate
• Kulmala (1996)- < 24h = 92% erectile function
• Bennett and Mulhall (2008)- 39 pts treated for ischemic
priapism
– 100% had spontaneous erections if < 12h
– 78% if between 12-24h
– 44% between 24-36h
– 0% if > 36h
99.
100. Treatment of NonIschemic Priapism
• Usually not painful.
• Rare compared to LFP
• Natural history is resolution
(vs. ED)
• Rarely NonIschemic Priapism
can occure after resolution of
ischemic priapism
• 62% resolve with conservative
tx (ice, compression)
• no comparative outcome
studies of intervention vs
conservative management
101. • Corporal aspiration has only a diagnostic role.
• Aspiration with or without injection of
sympathomimetic agents is not recommended as
treatment.
• Initial management of should be observation.
• Immediate invasive interventions (embolization or
surgery) can be performed at the request of the
patient,
• But before intervention discuss
– the chances for spontaneous resolution and
– risks of treatment-related erectile dysfunction
102. Doppler sonography for localization
of a fistula
Fistula blush along with normal
arteriograms
103. Embolization
• Agents used are microcoils, polyvinyl alcohol, N-butylcyanoacrylate,
gel-foam, and autologous blood clot.
• non-permanent (Autologous clot and absorbable gels), are
preferable to permanent agents
• Success rates - 89% to 100%
• recurrence rate - 30% to 40%
• Complications
– erectile dysfunction - 15 – 20%
– penile gangrene,
– gluteal ischemia,
– purulent cavernositis,
– abscess of the perineum
104. Surgical management of
NonIschemic Priapism
• It is reserved for patients
– who do not wish to pursue expectant management
– who are poor candidates for angio-embolization.
– for patients in places where technology is not available;
– for patients whose angio-embolization failed
• The surgical approach is transcorporal.
• Intraoperative Doppler ultrasound guidance is
recommended.
• ED – 50%
105.
106. Complications
• Untreated low-flow priapism leads to corporal fibrosis and
impotence
• Early complications:
• acute hypertension, headache, palpitations
• bleeding, haematoma, infection and urethral injury
• Late complications:
• fibrosis and impotence
• related to duration of priapism
• low-flow : high incidence of ED if not treated within 12 hours
• high flow : good prognosis (20% rate of ED)
107. Partial priapism
• It also known as partial
segmental thrombosis of
the corpus cavernosum, is a
rare urological condition.
• In world literature, only 34
cases have been described
and the condition's
aetiology and treatment are
still controversial.
• Bicycle riding, trauma, drug
usage, sexual intercourse,
haematological diseases
and α-blockers have been
associated with PP.
108. Female priapism
• The incidence of priapism in women
is not known but must be extremely
low since the only information from
the published literature is from case
reports, although underreporting
may be present since the condition
may be transient.
• The main mechanism of priapism
(male and female) consists of
impaired outflow from the corpora
cavernosa through direct venous
obstruction or failure of the alpha-
adrenergic relaxation system.
109. • This is reflected in the reported causes of female
priapism, which include malignancies and certain
medications, in particular, the drugs with marked
(alpha-)sympathetic blockade.
• Malignancies in association with female priapism
include local recurrence of bladder carcinoma
• Most reported cases of female priapism describe
the association with the use of antidepressant
and other psychotropic drugs, all with alpha-
adrenergic blocking potential, such as trazodone,
buproprion, citalopram and nefazodone
110. • Treatment in the case cited above consisted of
discontinuing the offending medication or providing
symptomatic pain relief.
• Serious permanent damage where treatment has been
delayed has been reported in men but not in women.
• Furthermore, the association between congenital
clitoromegaly and priapism has also not been reported
previously.
• With this concern in mind, but hitherto not for female
priapism, i.e. the direct injection with epinephrine and
heparin, followed by aspiration to provide immediate
decompression.
Penile erection is a complex neurovascular
event involving the interaction of three physiological
systems: the central nervous system (CNS), the peripheral
nervous system and the penile arterial and
trabecula smooth muscle
The penile corpora, a
specialized vascular tissue, consisting of endotheliallined
sinusoidal spaces supported by a framework of
smooth muscle, collagen, nerves, nutritive arterioles
and capillaries (4). Normal erectile function is a complex
interaction of both, the nervous and vascular
system. Erection requires relaxation of trabecula
smooth muscle that results in an increased compliance
of the sinusoids and arterial wall as well as a
dilatation of the arterioles and arteries.
Small for ischaemic long for non
Pain in ischaemic
After aspiration, a reactive hyperaemia may develop with a high arterial flow that may mislead the diagnosis as arterial priapism.
Penile arteriography may be used as an adjunctive study to identify the presence and site of a
cavernous artery fistula (ruptured helicine artery). Since color duplex ultrasonography has
largely supplanted arteriography for the diagnosis of cavernous artery fistulae, arteriography is
usually only performed as part of an embolization procedure
MR T1WI post contrast a) No enhancement in either corpora indicative of
a classical total infarction b) A different patient with bright enhancement surrounding
the cavernosal arteries and proximal perfusion (bright enhancement around proximal
cavernosal artery) but little net inflow with resulting infarction of the majority of the corporal
tissue.
The treatment options for penile anaesthesia/systemic analgesia include:
• dorsal nerve block;
• circumferential penile block;
• subcutaneous local penile shaft block;
the 3 o’clock and 9 o’clock
• oral conscious sedation (for paediatric patients).
drain stagnant blood from the corporal bodies, making it possible to relieve the compartment syndrome-like
condition of the penis.
The needle must penetrate the skin, the subcutaneous tissue and the tunica
albuginea to drain the corpus cavernosum
Aspirate 50 mL.If this does not lead to detumescence, then
another 50 mL is aspirated from the contralateral
corpus.
If failure, then another 50 mL should
be aspirated and irrigate with
30–40 mL warm, heparinised saline solution
(5000 U/L) and then aspirate another 30–40 mL
Some clinicians use two angiocatheters or butterfly needles at the same time to accelerate drainage, as well as
aspirating and irrigating simultaneously with a saline solution.
There are insufficient data to determine
whether aspiration followed by saline intracorporeal irrigation is more effective than aspiration alone
After injection, the puncture site should be
compressed and the corpora cavernosa massaged to facilitate drug distribution
Wait for 5–10 minutes; if this fails, then repeat the
injection with another 200 mg of phenylephrine. If
this fails, then consider another 500 mg of
phenylephrine.
the Panel recommends use of
phenylephrine because this agent minimizes the risk of cardiovascular side effects that are
more common for other sympathomimetic medications.
Phenylephrine use has potential cardiovascular side-effects and it is recommended that
blood pressure and pulse are monitored every 15 minutes for an hour after the injection. his is particularly
important in older men with existing cardiovascular diseases.
Overall, the administration of intracavernosal sympathomimetic agents is contraindicated in patients suffering
from malignant or poorly controlled hypertension
Sympathomimetic
A number of clinical
indicators suggest failure of first-line treatment including continuing corporal rigidity, cavernosal acidosis and
anoxia, absence of cavernosal artery inflow by penile colour duplex US, and elevated intracorporal pressures
by pressure monitoring
There is no evidence detailing the
amount of time allowed for first-line treatment before moving on to surgery. Consensus recommendations
suggest a period of at least 1 hour of first-line therapy prior to moving to surgery
In general, the type of shunt procedure chosen is according to the surgeon’s preference and procedure
Familiarity. It is conventional for distal shunt procedures to be tried before proximal shunting is
Considered
The same procedure above can be done using a scalpel.
The last resort in cases where the above mentioned shunts failed
communication between the corpus cavenosum and the corpus spongiosum. The most frequent complications
include an unwanted urethra-cavernous fistula and urethral stricture or the development of cavernositis
Intractable, therapy-resistant, acute ischaemic priapism or episodes lasting more than 48-72 hours usually
result in complete ED, possibly along with major penile deformity.
Colour doppler ultrasound showing a segmental thrombosis in the proximal corpus cavernosum.
Partial priapism usually resolves spontaneously with analgesic treatment while surgical intervention is rarely
needed
Cleveland Clinic, Center for Urogynecology and Reconstructive Pelvic Surgery, Obstetrics, Gynecology & Women's Health Institute, Cleveland, OH, USA
----- Meeting Notes (04/10/16 04:45) -----
circumcision, bucks fascia incised, tunica albuginea exposed, dorsal vein identified, corporotomy done, stay sutures near the corpora, dorsal vein sutured to corpora with 5.0 PDS
