The document discusses priapism, beginning with definitions and epidemiology. It then covers etiology, natural history, pathology, pathophysiology, classification, diagnosis, treatment, and complications of priapism. The key points are that priapism can be ischemic (low flow) or nonischemic (high flow) and treatment involves relieving the ischemia through aspiration or shunting for ischemic priapism or selective arterial embolization for nonischemic priapism.

1. Priapism
Dr Atef M Solimann
Urosurgeon
MBH
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2. Arterial supply
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3. Hemodynamics and Mechanism of Erection
and Detumescence
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4. Neuroanatomy and Neurophysiology of
Penile Erection
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5. Neuroanatomy and Neurophysiology of Penile Erection
cont.
Most researchers now agree
that NO released from
nonadrenergic,
noncholinergic
neurotransmission and from
the endothelium is the
principal neurotransmitter
mediating penile erection. NO
increases the production of
cGMP, which in turn relaxes
the cavernous smooth muscle
(Trigo-Rocha et al, 1993a, 1993b).
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6. • DEFINITION
• EPIDEMIOLOGY
• ETIOLOGY
• NATURAL HISTORY
• PATHOLOGY
• PATHOPHYSIOLOGY
• CLASSIFICATION
• DIAGNOSIS
• TREATMENT
• SUMMARY
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7. DEFINITION
• Is a pathologic condition of penile erection
characterized as prolonged and devoid of
sexual stimulation or excitement ( Berger et al,
2001 and Montague et al, 2003 ).
• Priapism of the clitoris has also been
described in the medical literature ( Monllor et
al, 1996 ).
• Pain is a common descriptor, perceived to
be a consequence of genital tissue
ischemia and increased pressure
generated within the corporal bodies,
although this feature is not a requirement
for the designation of priapism.
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8. EPIDEMIOLOGY
Cohort studies involving
populations with sickle
disease demonstrate
lifetime probabilities for
development of priapism to
be between 29% and 42%
(Adeyoju et al, 2002 ).
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9. ETIOLOGY
1- Hematologic
Dyscrasias
Sickle cell disease 23% of adult,
63% of pediatric cases, Leukemia
50% of patients with this disease,
Asplenism, Erythropoietin,
hypercoagulable states, total
parenteral nutrition containing 20%
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fat 9

10. ETIOLOGY cont.
2- Neurologic Conditions
Neurologic infections such as syphilis, brain tumors,
epilepsy, intoxication, and brain and spinal cord injury
( Hinman, 1914 and Munro et al, 1948 ).
Anesthesia, either general or regional (spinal or epidural)
administration, with genital manipulation as part of the
surgical procedure
(Shantha et al, 1989 and Dittrich et al, 1991 ).
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11. ETIOLOGY cont.
3- Nonhematologic Malignant
Neoplasms
Local primary or metastatic neoplastic processes are also
known to carry priapism risks. Organs of cancer origin
include penis, urethra, prostate, bladder, kidney, and
rectosigmoid colon
(Morga Egea et al, 2000 and Hettiarachchi et al, 2001 ).
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12. ETIOLOGY cont.
4-Trauma
Priapism has been associated with direct
penile and perineal trauma (straddle injury
or direct scrotal trauma) ( Burt et al, 1960 ;
Hinman, 1960 ) as well as traumatic needle
insertion with intracavernosal
pharmacotherapy ( Witt et al, 1990 ).
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13. ETIOLOGY cont.
5- Erectile Dysfunction
Pharmacotherapy
Lomas and Jarow (1992) defined the risk profile of priapism
in this setting, finding that younger men with better baseline
erectile function, patients with overt neurologic disease, and
patients without significant cardiovascular disease were
most susceptible.
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14. ETIOLOGY cont.
6- Pharmacologic Exposures
A- Antihypertensive agents:
Hydralazine and guanethidine ( Rubin, 1968 ) and α-adrenergic antagonists
(Vaidyanathan et al, 1998 ).
B- Psychotropic and antidepressant medications:
Phenothiazines, sedative-hypnotics, SSRI, and trazodone (Compton and Miller,
2001 ).
C- Other medications:
Heavy alcohol intake (Kulmala et al, 1995b), Topical and intranasal cocaine
administration (Altman et al, 1999 ), Immunosuppressant agent FK506
(tacrolimus) ( Harmon et al, 1999 ), androgen supplements (Zargooshi, 2000 ),
and scorpion toxin ( Teixeira et al, 2004 ).
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15. ETIOLOGY cont.
7- Idiopathic
Some investigators have estimated that this
disorder accounts for as many as half of all
documented cases ( Larocque and Cosgrove, 1974 ;
Pohl et al, 1986 ; Winter and McDowell, 1988 ).
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16. NATURAL HISTORY
• Outcome: is either its permanent resolution
or its progression to recurrent episodes with
or without some degree of erectile
impairment.
• In the absence of effective treatment, it has
long been recognized that even major
episodes of ischemic priapism will
eventually resolve in time, although
permanent damage of the penis may be
expected.
• It is perceived that individuals with
nonischemic priapism generally preserve
erectile ability.
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17. PATHOLOGY
• Penile tissue necrosis and progressive
fibrosis are the end-stage
manifestations of ischemic priapism, (
Hinman, 1960 ).
• The irreversible effects resulted
most consistently from the
combination of hypoxia, acidosis,
and glucopenia at a time interval
of 4 hours (Muneer and
associates, 2005) .
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18. PATHOPHYSIOLOGY
• Vascular stasis in the penis and decreased
venous outflow from the organ were the
primary circumstances that mechanically or
physically interfered with detumescence
( Hinman,1960).
• Fistula formation (cavernous artery and lacunar
spaces of the cavernous tissue), which allows
blood to bypass the normal cavernous
arteriolar bed, then accounts for
traumatically induced priapism (Hakim et
al, 1996).
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19. CLASSIFICATION
• Ischemic (low flow) Priapism
• Nonischemic (high flow) Priapism
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20. CLASSIFICATION cont.
Priapism Variants
1- Recurrent (Stuttering) Priapism
2- Refractory Priapism
3- Neurogenic Priapism
4- Idiopathic Priapism
5- Drug-Induced Priapism
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21. DIAGNOSIS
History
Pain, duration of priapism (< or >4hrs), prior priapism, use and
success of relieving maneuvers or prior clinical treatments,
existence of etiologic conditions, and erectile function
status before the priapism episode.
Physical Examination
Inspection and palpation of the penis:
extent of tumescence or rigidity, corporal body involvement
(i.e., whether rigidity involves only the corpora cavernosa
with a soft glans penis and corpus spongiosum or all three
corporal bodies).
Abdominal, perineal, and DRE may reveal signs of trauma or malignant
disease.
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22. DIAGNOSIS cont.
Laboratory Testing
CBC, white blood cell differential, and platelet count
(acute infections or hematologic abnormalities).
Reticulocyte count and hemoglobin electrophoresis
(sickle cell disease or trait and hemoglobinopathies)
Screening for psychoactive drugs and urine
toxicology to identify overdoses of legal and illegal
drugs may also be performed.
Berger et al, 2001 ; Montague et al, 2003
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23. DIAGNOSIS cont.
Penile Diagnostics
1- Aspirates should be visually inspected
Patients with ischemic priapism, the blood is
hypoxic and therefore dark, whereas that of
patients with nonischemic priapism is oxygenated
and therefore bright red.
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24. DIAGNOSIS cont.
Penile Diagnostics cont.
2- Cavernous blood gas testing
• Normal flaccid penis cavernous blood gas levels:
normal mixed venous blood at room air (Po2 of 40 mm
Hg, Pco2 of 50 mm Hg, and pH of 7.35) ( Montague et al,
2003 ).
• Cavernous blood gas in patients with ischemic
priapism: Po2 <30 mm Hg, Pco2 >60 mm Hg, and pH
below 7.25
• Cavernous blood gas in patients with nonischemic
priapism (normal arterial blood at room air ): Po2 > 90
mm Hg, Pco2 < 40 mm Hg, and pH of 7.40 (Montague et
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al, 2003 ).

25. DIAGNOSIS cont.
Radiologic Evaluation
1- Color duplex ultrasonography
(lithotomy or frogleg position, scanning the perineum first and then the entire
penile shaft).
Ischemic priapism have minimal or absent blood flow in
the cavernosal arteries and the corpora cavernosa.
Nonischemic priapism have normal to high blood flow
velocities in the cavernosal arteries and the corpora
cavernosa.
Anatomic abnormalities: cavernous arterial fistula or
pseudoaneurysm, to confirm the diagnosis of nonischemic
priapism.
(Hakim et al, 1996 ).
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26. DIAGNOSIS cont.
Radiologic Evaluation cont
2- Arteriography:
Not routinely used for diagnosis
and is otherwise usually
performed as part of an
embolization procedure.
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27. TREATMENT
I- Ischemic Priapism
In general, since ischemic priapism of more than 4
hours in duration irrespective of etiology implies a
compartment syndrome, decompression of the
corpora cavernosa is recommended for
counteracting the ischemic effects including pain
sensations (Montague et al, 2003 ).
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28. TREATMENT cont.
Winter shunt
1- Dorsal nerve block or local penile shaft block ( Berger et al,
2001 ).
2- Transglanular intracorporal needle insertion with an
angiocatheter (16- or 18-gauge).
3- Evacuation of blood and irrigation of the corpora cavernosa with
intracavernous injection of an α-adrenergic sympathomimetic
agent ( Montague et al, 2003 ).
4- Repeated aspirations or irrigations and sympathomimetic
injections during several hours may be necessary and should be
performed before initiation of surgical intervention.
5- Sickle cell disease: analgesia, hydration, hyperbaric
oxygenation, alkalinization, and transfusion if prolonged periods
of ischemia have occurred ( Mantadakis et al, 2000 ).
6- Priapism resolution 30% ( Montague et al, 2003 ).
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29. TREATMENT cont.
1- Sympathomimetics (α-adrenergic agents)
contractile effects on the cavernous tissue
(Blood pressure and ECG monitoring in patients with
high cardiovascular risk) (Montague et al, 2003 ).
A- Phenylephrine:
α1-selective adrenergic agonist < the risk of
cardiovascular side effects, 100-200 mg
every 5-10 min until detumescence
(maximum 1000 μg)
B- Epinephrine α, β agonist 10-20 μg every 5-10 min
until detumescence
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30. TREATMENT cont.
2- Antiandrogens (Hormonal)
A-Gonadotropin-releasing hormone agonist,
Leuprolide 7.5 mg once a month IM
B- Androgen receptor antagonist, Oral tablets
Bicalutamide 50 mg once a day
Flutamide 250 mg every 8 hours
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31. TREATMENT cont.
3- Miscellaneous
Oral tablets
Baclofen γ-Aminobutyric acid agonist, 20-40 mg once a day
(bedtime)
Digoxin Cardiac glycoside, 0.5 mg every day
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32. TREATMENT cont.
Surgical shunt
Indications
1- Intracavernous treatment has failed.
2- Extended durations (48 to 72
hours).
( Montague et al, 2003 )
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33. TREATMENT cont.
Surgical shunt cont.
1- Distal cavernoglanular
• A- Winter shunt: Travenol biopsy needle ( Winter, 1976 ).
• B- El-Ghorab shunt : excision of the tunica albuginea at
the tip of the corpus cavernosum ( Ercole et al, 1981 ).
El-Ghorab procedure is regarded as the most effective distal shunt,
although it is more invasive and thus commonly performed
secondarily ( Montague et al, 2003 ; Nixon et al, 2003 ).
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34. TREATMENT cont.
Surgical shunt cont.
2- Proximal shunting
A- Sacher shunt:
By creation of a window
between the corpus
cavernosum and corpus
spongiosum
(Sacher et al, 1972 )
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35. TREATMENT cont.
Surgical shunt cont.
Proximal shunting cont.
B- Grayhack shunt:
By anastomosis of the saphenous
vein to one of the corpora
cavernosa ( Grayhack et al, 1964 )
May be warranted if distal
shunting fails.
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36. TREATMENT cont.
Complications
Urethral fistulas
Purulent cavernositis
Pulmonary embolism
( Kandel et al, 1968 ).
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37. TREATMENT cont.
II- Nonischemic Priapism
The initial management of
nonischemic priapism should be
observation (Montague et al, 2003 ).
Selective arterial embolization offers
the next step for the patient desirous
of an immediate resolution.
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38. TREATMENT cont.
Nonischemic Priapism cont.
Embolization materials
• Nonpermanent (autologous clot, absorbable gels).
• Permanent (coils, ethanol, polyvinyl alcohol particles,
and acrylic glue)
(75% resolution rate)
Nonpermanent materials are preferred as
producing a lesser ED rate (5% versus 39%
with permanent substances) ( Montague et al,
2003 ).
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39. TREATMENT cont.
III-Recurrent (Stuttering) Priapism
All episodes of recurrent priapism should be
treated like ischemic priapism ( Montague et
al, 2003 ).
Systemic therapies (hormonal agents , baclofen,
digoxin) or intracavernous self-injection of
sympathomimetic agents, and penile prosthesis
surgery.
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40. TREATMENT cont.
Miscellaneous Medical Therapies
• hydroxyurea in the treatment of sickle cell-
associated priapism
• Thrombolytics such as streptokinase ( Gibel
et al, 1985 ) and tissue plasminogen
activator ( Rutchik et al, 2001 ) for ischemic
priapism
• Methylene blue for high-flow priapism
( Steers and Selby, 1991
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41. SUMMARY
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42. Thank u
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