3. DEFINITION::
➢ full or partial sustained erection
➢ > 4hrs
➢ Absence of physical or psychological stimulation
Usually,
• Painful
• Tumescense is restricted to corpora cavernosa
5. EPIDEMIOLOGY:
⚫ Reports on the epidemiology and cause of priapism are
greatly influenced by prevalence of sickle cell disease in the
population described.
⚫ The lifetime probability of man with SCD developing
ischemic priapism ranges from 29-42%.
⚫ The mean age at time of hospital admission a/s with SCD
was 23.8yrs and for non-SCD was 40.8yrs.
⚫ Sickle cell diagnosis was associated with 57% of pediatric
admissions and 20% of adult admissions.
7. ISCHEMIC PRIAPISM
(veno-occlusive, low flow)
⚫ It is most common form and also most serious and dangerous b/c of
the acute ischemia of CC
⚫ It is a persistent erection marked by rigidity of the CC and little or no
cavernous arterial inflow.
⚫ There are time dependent changes in the corporal metabolic
environment with progressive hypoxia, hypercarbia and acidosis.
⚫ Patient typically complains of penile pain after 6 to 8 hrs and
examination reveals a rigid erection.
⚫ Interventions beyond 36hrs of onset may help relieve erection and
pain but have no benefits in preserving potency.
⚫ When left untreated resolution may take days to wks and sever
corporal fibrosis and erectile dysfunction invariably result.
8. Pathophysiology:
⚫ Erection may begin with sexual stimulation or the administration of
pharmacologic agents.
⚫ Once erection persist beyond 4hrs and not relived by orgasm or
pharmacological reversal, the mechanism of ischemic priapism begun.
⚫ Outcome and seriousness is directly related to severity of the obstruction
and duration of the blockage of drainage of CC.
⚫ Decrease in venous outflow and vascular stasis cause tissue hypoxia,
anoxia and acidosis.
⚫ Hypoxia and acidosis begin after 4hrs and increase to peak levels in
24hr.
9. • Penile pain occurs with significant tissue hypoxia.
• It leads to loss of contractility of cavernous smooth muscle.
• Histological changes:
- edema of cavernous tissue
- destruction of sinusoidal endothelium
- exposure of basement membrane
- adherence of thrombocytes
- anoxia and necrois of cavernous smooth muscle
Leads to
irreversible
fibrosis that result
in ED
10. • SCD priapism has traditionallybeen ascribed to stagnation of bloodwithin
sinusoids of the CC during physiologic erection, secondary to obstructionof
venous flow by sickled erythrocytes.
• Accountsfor at least one-thirdof all cases.
• Mean age of onset of priapism is 15yrs.
• 75% of pts having 1st episode before age 20yr.
• Precipitatingevents were sexual arousal or intercourse, fever, sleep, cold
weather and dehydration.
• 72% of pts had Hx of stutteringpriapism, three times per month, mean
duration of each episode was 1.2hr.
SICKLE CELL DISEASE:
11. Pathophysiology:
• Hemolysis releases Hbg into plasma.
• Free Hbg reacts with NO to producemethemoglobin and nitrate.
• This is scavenging reaction, the vasodilator NO is oxidized to inert nitrate.
• Sickled erthrocytes release arginase-I into blood plasma, which converts L-
arginine into ornithine, effectively removing substrate for NO synthesis.
• Oxidant radicals further reduce NO bioavailability.
• State of NO resistance and insufficiency termed hemolysis-associated
endothelial dysfunction.
• Hemolysis and reduced NO responsible for priapism where as increased
blood viscosity responsiblefor painful crises.
• Also seen in the pathogenesis of pulmonaryHTN, leg ulcers, stroke
12. • SCD priapism associated with
- Hb
- Hemolytic markers (reticulocytecount, bilirubin,LDH and
AST)
• Cerebral vascular accidents are more frequent, close to episode of full-blown
priapism.
• ASPEN syndrome (association of SCD, priapism, exchange transfusions and
neurologic events)
13. • ICI remains an important therapeuticoption for men with severe ED.
• Prolonged erection most commonly reportedthan priapism after ICI.
• Most common of these drugs are papaverine, prostaglandin E1 (PG1),
phentolamineand moxisylate.
• Most of these cases priapism result from an over dosage of these drugs.
• Incidence is less with PG1 or combinition than papaverine alone.
IATROGENIC PRIAPISM:
(INTRACAVERNOUSINJECTIONS)
14. • Few case reportspriapism after Phosphodiesterase(PDE) type 5
inhibitortherapy.
• Methyphenidate and atomoxetine medications used in treatment of
ADHD result in prolonged erection or priapism.
ORAL MEDICATIONS:
15. • Stuttering(intermittent)priapism describes a pattern of recurrent priapism.
• Traditionally, its been used to describe recurrent unwanted and painful
erections in men with SCD.
• Patient awakens with an erection that persists up to 4hrs and becomes
progressively painful secondaryto ischemia.
• SCD pts may experience stutteringpriapism from childhood.
• Pts will experience repeated painful intermittent attacks upto several hours
before remission.
STUTTERING PRIAPISM:
16. • Commonly reported precipitants of full blown SCD priapism are stuttering noctural or
early morning erections.
• SRE take place during REM sleep and its androgen dependent.
• SCD pt complain of SRE lasting 3 to 4hrs and associated with pain.
17. • Persistent erection caused by unregulated cavernous arterial inflow.
• It is much rare than ischemic priapism and mostly related to trauma.
blunt or penetratingresulting in laceration of the cavernous artery or
one of its branches.
• Most common cause is straddleinjury to the crura.
• Coital trauma
• Kicks to penis or perineum
• Pelvic fracture
• Birth canal trauma to newborn male
• Vascular erosions complicating metastatic infiltration of corpora.
NON-ICHEMIC PRIAPISM:
(High Flow Priapism)
18. ⚫ Although accidental blunttrauma is most common cause but HFP occurs
after iatrogenic injury:
− Cold-knife urethrotomy
− Nesbitt corporoplasty
− Deep dorsal vein arterialization
⚫ Aggressive management of ischemic priapism (ɑ-adrenergic
injection/aspirationor shunting) converts LFP to HFP.
⚫ CDU shows arteriolar-sinusoidal fistula at the site intervention.
19. Pathophysiology:
• Laceration of cavernous arterioleproduceunregulated poolingof blood in
sinusoidal space with consequent erection.
• HFP typicallydelayed in onset compared with episode of trauma (may
develop after 24hrs of perineal or penileblunt trauma.)
• Unregulated arterial inflow creates a arteriole-lacunarfistula.
• Fistula forms pseudocapsule(take several wks to months).
• Non-fistula type of arterial priapism is the result of dysregulation of
cavernous inflow, post-ischemic hyperemia.
20. ⚫ SecondaryHFP should be suspected in pts with
− Rapid recurrence
− Persistence erection with partial penile rigidity
− Not associated with pain
⚫ Non-fistula arterial priapism is rare complication after management of
ischemic priapism.
⚫ Dysregulated arterial inflows with or without a fistula can be distinguished
from persistent ischemic priapism by CDU.
21. PRIAPISM IN CHILDREN:
⚫ Most commonly related to SCD 65%, leukemia10% and trauma 10%.
⚫ Incidence is 2-6%.
⚫ Majority of cases have been conservatively managed with spontaneous
resolution.
⚫ CDU should be performed.
⚫ In children with hx of trauma, arteriolar-sinusoidal fistula must be localized.
⚫ Direct manual compression softens the high-flow erection and may speed
spontaneousresolution.
⚫ Conservative management works in children due to less subcutabeous fat
and easily compressible crural bodies.
⚫ HFP may spontaneously resolve or respond to perineal compresion and
icing.
22. EVALUATION AND DIAGNOSIS:
⚫ HISTORY:
− Physician must determine whether priapism is ischemic or non-ischemic.
− Duration of erection
− Presence of pain
− Previous episodes of priapism and its treatment
− Use of any erectogenic therapies
− Medications
− SCD, hemoglobinopathies, hypercoagulable states
− Trauma to pelvis, perineum or penis.
23. ⚫ PHYSICAL EXAMINATION
− Extent and degree of tumescence
− Rigidity
− Presence of pain
− Evidence of trauma
− Examination of abdomen, testicles, perineum, rectum and prostate for
malignancy.
⚫ In ischemic priapism corporal bodies will be completely rigid, the glans penis
and corpus spongiosum are not.
⚫ In nonischemic priapism the corpora will be tumescent but not completely
rigid.
24. LABORATORY TESTING:
⚫ CBC and coagulation profile.
− To access anemia and rule out infection or hematologic abnormalities.
⚫ Hemoglobin electrophoresis, reticulocyte count and LDH.
⚫ Corporal blood apiration (diagnostic and therapeutic)
⚫ Visual inspection of color and consistency of initial aspirate will reveal dark
deoxygenated blood with crankcase oil appearance in ischemic priapism.
⚫ Aspirate sent for blood gas testing to see pH, PO2 and PCO2.
25. PENILE IMAGING:
ColourDopplerUSG:
− Recommended in evaluation of priapism.
− Is an adjunct to corporal aspirate in
differentiating ischemic from non-
ischemic.
− Differential diagnosis includes resolved
ischemia with edema, persistent ischemia
and conversion to high-flow state.
− In ischemic priapism: no blood flow in
cavernous arteries.
− In non-ischemic priapism: normal to
high blood flow in cavernous arteries.
26. MRI
− It has three possibleroles
1. Imaging of well-established arteriolar-sinusoidalfistula
2. Presence and extent of tissue thrombusand corporalsmooth muscle
infarction
3. Corporal malignancy or metastasis.
ARTERIOGRAPHY
• Penile arteriography should be reserved for the management of HFP,
when embolization is planned.
• It is too invasive as a diagnostic procedure.
27. MEDICAL TREATMENTS:
⚫ First aid : ice packs, cold baths, cold water enemas, voiding, ejaculation
and exercise.
⚫ Oral sympathomimetic drugs (pseudoephedrine, phenylpropanolamine
and terbutaline)can effectively reverse prolonged erection <4hrs.
⚫ Oral medications not recommended in the management of acute
ischemia (>4hrs).
⚫ Initial treatment for ischemic priapism is decompression of CC by
aspiration.
28. ⚫ Aspiration will immediately soften the erection and relieve pain.
⚫ Aspiration alone may relieve priapism in 36% cases.
⚫ Aspiration + intracorporal saline irrigation will be more effective.
⚫ Aspiration should be repeated until fresh bright red bloodobtained.
⚫ This will lead to decrease in intracavernous pressure, pain relief and
removes anoxic, acidotic, and hypercarbic blood.
29. ⚫ A single, large-bore, 19 gauge
needleshould be inserted at
peno-scrotaljunction at the 3 or
9 o’clockposition to avoid
piercing dorsal neurovascular
bundle.
⚫ Compress penile shaft between
thumb and first digit, just below
needle.
⚫ Aspirate the shaft until it is soft.
⚫ Needle left in place, shaft is
permitted to refill and repeat
mneuvers.
⚫ Corporal aspiration, if
unsuccessful, should be followed
by ɑ-adrenergic injection (AOC)
or irrigation.
30. Phenylephrineis dilutedis normal saline to a concentrationof 100-200µg/ml.
It is administered intracavernouslyas a 1ml injection every 3 to 5 minutes.
It should be intermittent over an hour with maximum dose of 1mg.
Monitorbloodpressure and pulse rate during and immediately after ICI.
Side effects: headache, dizziness, hypertension,reflex bradycardia, tachycardia and
Cardiac arrhythmia.
Contraindications:uncontrolledHTN, monoamine oxidase inhibitor.
31. ⚫ Treatment of SCD-induced ischemic priapism involved analgesics,
hydration, oxygen, bicarbonate and exchange transfusion.
⚫ Hematologists emphasis on I/V hydration, sodium bicarbonatefor
alkalinizationand exchange transfusion as first line treatment for SCD-
associated priapism.
⚫ Hydroxyurea is used in management of vaso-occlusive crisis of SCD.
⚫ High success rates seen with penile aspiration, injection and irrigation with
intra-cavernnoussympathomimetic for SCD priapism.
32. Stuttering priapism:
⚫ Goals of treatment:
o prevention of future episodes,
o preservation of erectilefunction and
o balancingrisks versus benefits of various treatment options.
⚫ Multipletreatment optionshave been described:
− oral and injectable ɑ-adrenergic agonists, terbutaline, antisickling agents
hydroxyurea, gonadotropin-releasing hormone (GnRH) analogues,
antiandrogens, baclofen and recentlyPDE5 inhibitors.
⚫ Limited daily administration of oral drugs should be considered typically
initiated at bedtime.
33. ⚫ To treat stutteringpriapism with hormonesis by targeting:
− pituitarygland (GnRH agonists), suppressing pituitaryfunction through
feedback inhibition (diethystilbestrolDES), blockingandrogens
receptors(antiandrogens)and reducingtesticularand adrenal synthesis
(ketoconazole).
⚫ The goal of hormonal therapyis to reduceserum testosteroneto
hypogonadal level or block testosterone’seffects on the penis.
⚫ Antiandrogenshave benefit over GnRH analogues----they are orally
adminitered.
34. Baclofen: inhibitspenile erection and ejaculation through γ-
aminobutyricacid (GABA) receptorsactivity.
⚫ 40mg oral nightly can be used in management of recurrentpriapism
in pts with neurologic lesions.
⚫ Withdrawal syndrome characterizedby return of spasticity, agitation,
sleeplessness and priapism.
35. SURGICAL MANAGEMENT OF ISCHEMIC
PRIAPISM
⚫ If conservative measures are unsuccessful, then a surgical approach may be
necessary.
⚫ Goal of surgical management is to allow blood flow in and out of the penis
freely to prevent ischemia and fibrosis of the penis.
⚫ Principles of most of the priapism surgeries involve creation of fistula
between engorged corpus cavernosum and glans, corpus spongiosum and
dorsal or saphenousveins.
⚫ Counseledregarding erectilefunction outcome-
complete ED if LFP persistsfor longerthan 36hrs.
36. SHUNTING:
⚫ Shunt proceduresare subdivided on the basis of anatomic locationof penis.
⚫ Distal cavernoglandular shunt should be the first choice of shunting
procedures.
⚫ Shunting is to be considered for ischemic priapism events lasting 72hrs or
less.
⚫ Objective of shunt surgery is reoxygenation of cavernous smooth muscle.
⚫ Reestablish corporal inflow by relieving outflowobstruction.
⚫ It requires creation of fistula b/w CC and glans penis, CC and CS or CC and
dorsal or saphenousvein.
⚫ Percutaneous distal shunting is less invasive and can be performed in local
anesthesia in ER.
38. Winter Shunt:
⚫ Distal cavernoglanular shunt
procedure is created by transglanular
placement of a large-bore needle or
angiocatheter into distal galns and CC.
⚫ A core of tunica albuginea separeting
the glans and the CC removed with
needle thus creating a fistula.
39. Ebbehoj Shunt
⚫ A glans-cavernosal shunt is made with
n0 11 blade.
⚫ Straight incision into glans and corpus
cavernosum is given.
⚫ Deoxygenated blood is milked out of
open incision, once bright red blood is
seen, the skin is closed.
⚫ Leaving deeper incision open surgical
fistula.
40. T- Shunts
⚫ T-shaped glans-cavernosal shunt using
a n0 10 scalpel.
⚫ The blade is inserted into each corpus
cavernosum from the glans, turned 90
degree away from urethra and then
pulled out to create a T-shaped shunt.
⚫ Deoxygenated blood is milked out of
open incision, once bright red blood is
seen, the skin is closed.
41. Al-Ghorab shunt
• Open corporoglanular shunt is indicated
if percutaneousshunting fails to
reestablish blood in flow.
• It requires the excision of circular cone
segments of the distal tunica albuginea
(5*5mm).
• Transverse incision is made on dorsal
aspect of glans approximately 1cm.
• When detumescence occurs skin is
closed.
42. Corporal Snake “Burnett”
• It is modification of Al-ghorab shunt.
• Rather than excising a wedge of tunica
and underlying CC muscle 7/8 hegar
dilator is advanced through each of
tunica windows proximally to release
blood and thrombus.
• Penis is made flaccid by repeated
manual compression and release.
• Glans skin is approximated and urethral
catheter placed.
43. Proximal shunts and venous bypass
• If distal shunts fails, then proximal
shunting is recommended to establishes
a communication b/t CC to CS at base
of penis.
• It requires trans-scrotal or transperineal
approach.
• Carry higher risk of urethral injury.
44. Venous Bypass
Grayhack Cavernoso-Saphenous shunt:
⚫ Saphenous vein is mobilized by
dividing and ligating the trubutaries.
⚫ Saphenous vein is spatulated and
anastomosed to CC.
Barry cavernosa-Dorsal Vein Shunt:
⚫ Also know as DDV shunt.
⚫ Distal ligation of DDV and
anastomosis of proximal DDV to CC.
45. • Key factors for determining successful surgical reversal of ischemic priapism
are
- evacuation of thrombus
- reestablishing of cavernous inflow
- Patency of shunt
• Assessing of shunt patency:
- visualization of bright red blood in corporalaspirate
- corporal bloodgas
- color dopplerultrasonography
- measurement of intracavernouspressure
- Penile compression maneuver (squeeze and release)
47. To prevent shunt obstruction and failure:
1. Avoid compressive penile dressing
2. Periodic squeeze and release distal penis to milk the shunt maintaining
patency.
3.Anticoagulation( preoperative aspirin 325mg coupled with subcutaneous
heparin 5000unitsand postoperative asprin 81mg daily for 2 wks.)
48. Penile prosthesis
• Natural history of untreated ischemic priapism or priapism refractory to
interventionsis severe fibrosis, penile length loss and completeED.
• Use in management of acuteischemic priapism when other procedurefailed.
• Main advantages to immediate implantation is corporal fibrosis is not yet
established and penile length may be preserved, and it is technicallyeasier.
• Complications:
• Infection
• Urethral injury
• Device migration
• Device erosion
49. MANAGEMENT OF NONISCHEMIC PRIAPISM:
• It is not an emergency.
• Spontaneousresolutionor response to conservative therapy.
• Partial erection resolved in 4 days and normal erection 2wks later.
• Cavernous aspiration has only diagnostic role in HFP.
• Patient demanding immediate relief: selective arterial embolization offered.
• Selective pudendal artery embolizationhas highest success rate (89% to
100%).
• In case of long-standingpriapism in which pseudocapsuledeveloped around
fistula surgical ligation is successful.
• CDU guidance is recommended during exploration to locate fistula.
