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D. Kandasamy and K. Kabilan
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Endovascular Interventions forMale
Infertility
SuryaPratapSingh, SreenivasaNarayanaRaju,
PriyaSingh, andS.H.Chandrashekhara
32
Key Messages
1. High-ow priapism, frequently resulting from traumatic
arteriolacunar stulas, requires early intervention.
2. Super-selective embolization offers superior outcomes
compared to conservative management, with the potential
for erectile function preservation when meticulously
targeted.
3. A comprehensive pre-procedural workup, including psychological, neurological and hormonal assessments, is
crucial for excluding the non-vascular causes.
4. Although duplex USG provides valuable initial vascular
insights, cavernosography provides the denitive diagnosis for veno-occlusive dysfunction.
5. Internal pudendal angiography and angioplasty hold the
potential for carefully selected patients with conrmed
vascular ED.
6. An understanding of the penile vascular anatomy, embolic
agents, techniques of sclerosant injection and potential
complications is vital in ensuring a good outcome after
the procedure.
7. Outcome tracking using validated measures, such as the
IIEF-5 questionnaire, assists in objectively evaluating the
success of the intervention.
8. Although promising, endovascular interventions for ED
warrant further research to determine their long-term efcacy and to optimize the patient selection.
S. P. Singh (*) · P. Singh
Department of Radiodiagnosis, King George’s Medical University,
Lucknow, India
S. N. Raju
Vascular and Neuro Interventional Radiology, Valluvanad Hospital
Complex, Ottapalam, Kerala, India
S. H. Chandrashekhara
Department of Radiodiagnosis and Interventional Radiology,
IRCH, All India Institute of Medical Sciences, Delhi, India
32.1 Introduction
While super-selective embolization of terminal internal
pudendal artery branches offers reliable treatment for highow arterial priapism, the use of vascular imaging and interventions, such as internal pudendal angiography and
angioplasty, in erectile dysfunction (ED) remains a topic of
debate. This chapter aims to give an insight on these topics.
32.2 Priapism
Priapism refers to prolonged, persistent erection unrelated to
sexual desire. This condition arises from an imbalance
between penile arterial inow and venous outow within the
corpora cavernosa. Although relatively uncommon in the
general population (incidence of 0.5–2.9 cases per 100,000
person-years), certain medical conditions are associated with
high risk of priapism. The risk factors include sickle cell
anaemia and the use of intracorporal injection-based ED
medications [1, 2].
Priapism can be broadly categorized into two distinct
types (Table32.1):
• Low-Flow/Ischaemic/Venoocclusive Priapism
– Incidence: Most common type.
– Aetiology: Can stem from prothrombotic disorders,
neurogenic causes, medications (including intracavernous vasodilators for ED), post-embolization or surgical intervention for venous leak. It can also be
idiopathic.
– Pathophysiology: Reduced blood outow due to
venous thrombosis triggers a compartment syndromelike process, which can result in penile gangrene.
– Clinical Presentation: Acute onset of intense pain
and rigidity are the usual symptoms. Aspiration tests
reveal venous blood from the corpora cavernosa.
Doppler studies typically show either no ow or slowow velocities within the cavernosal arteries.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
S. H. Chandrashekhara (ed.), Textbook of Interventional Radiology, https://doi.org/10.1007/978-981-97-9601-4_32
403
404
Table 32.1 Differential diagnosis of priapism
Type Aetiology Clinical features Diagnostic considerations
Low ow (ischaemic) Thrombosis, sickle cell anaemia,
medications
High ow (arterial) Trauma-induced stula, idiopathic Less painful, often delayed onset Arterial blood on aspiration,
Table 32.2 Diagnostic modalities for erectile dysfunction and high- ow priapism
Modality Use in erectile dysfunction Use in high-ow priapism
Duplex USG First-line diagnostic tool Assesses arterial and venous ow
Digital subtraction angiography “Gold standard” for vascular assessment Identies source of abnormal arterial ow
MRI Limited initial role; used for tissue
characterization
Acute onset of severe pain, rigid
corpora
Identies arterio-cavernosal stulas
Venous blood on aspiration, low/no
ow on Doppler
normal/high ow on Doppler
S. P. Singh et al.
– Management: It is a medical emergency requiring
urgent intervention (within 24hours) to avert necrosis
and irreversible ischaemia. It is typically managed by
an urologist with interventions including aspiration/
decompression, sympathomimetic agents and surgical
shunting if necessary. Specic protocols exist for priapism associated with sickle cell anaemia.
• High-Flow/Non-ischaemic/Arterial Priapism
– Incidence: It is less common as compared to the low-
ow form. Between 80 and 90% of non-traumatic
adult cases result from a single stula formation.
Children often present with multiple stulas [3].
– Aetiology: Trauma (particularly straddle injuries of
the perineum) is the most frequent cause, although it
can develop as a complication of low-ow priapism
complication or may have no recognizable trigger
(idiopathic) [4, 5].
– Pathophysiology: Dysregulated arterial ow develops
through an arteriolacunar (not typical arteriovenous)
stula connecting a branch of the internal pudendal
artery (usually cavernosal) with the lacunar spaces of
the corpora cavernosa. Outow remains unobstructed,
resulting in continuous inow/outow and preventing
blood pooling. Endothelial shear forces from this pattern promote nitric oxide release and cyclic guanosine
monophosphate pathway activation, perpetuating
smooth muscle relaxation [6, 7].
– Clinical Presentation: Unlike low-flow cases, pain
and ischaemia are not characteristic. Onset is typically delayed after the trauma but should be readily
apparent within 72hours. Corpora cavernosa aspiration yields arterial blood, and Doppler studies
often indicate normal or elevated cavernosal artery
velocities. Precise visualization of the arteriolacunar fistula site is also possible on Doppler USG
(Table32.2) [3].
– Management: Though American Urological
Association (AUA) guidelines suggest conservative
management initially with 62% spontaneous resolution rate, early embolization of the stula likely results
in more favourable outcomes [4].
32.3 Erectile Dysfunction
32.3.1 Denition
Erectile dysfunction (ED) is the inability to establish or sustain an erection rm enough for satisfactory sexual activity
[8].
32.3.2 Epidemiology
ED is highly prevalent and exhibits strong associations with
various underlying conditions [9–11]:
• Affects one-third of men at some point in their lives and
over 150 million men worldwide.
• Diabetes mellitus presents a threefold increased risk of
ED.
• Prevalence is linked to age: 12% in men aged <60years,
22% in men aged 60–69 years, and 30% in men aged
>70years.
• Other risk factors include hypertension, vascular disease,
dyslipidaemia, hypogonadism and depression.
32.3.3 Aetiology
Erectile dysfunction can have organic, psychological, or
combined origins (Table32.3). Potential causes include:
32 Endovascular Interventions forMale Infertility
Table 32.3 Aetiology and clinical presentation of erectile dysfunction
Etiological factor Description Clinical impact
Vasculogenic causes Arterial insufciency, venous leak Primary cause in many cases; often associated with
cardiovascular diseases
Neurological causes Spinal cord injuries, neuropathies Affects nerve signals necessary for erection
Hormonal imbalances Low testosterone levels, thyroid disorders Can reduce libido and impair erectile function
Psychological factors Stress, anxiety, depression Psychological state plays a signicant role in
sexual performance
Drug induced Antihypertensives, antidepressants Some medications can have side effects that impair
erectile function
405
• Vascular: Compromised blood ow due to arterial stenosis or venous leakage
• Neurogenic: Disruption of neural pathways involved in
erectile response
• Hormonal: Imbalances affecting erectile function
• Anatomic: Structural penile abnormalities
• Drug-Induced: Side effects of various medications
32.3.4 Pathophysiology
A typical sexual erectile response results from parasympathetic stimulation that triggers endothelial nitric oxide production. Nitric oxide, in turn, promotes smooth muscle
relaxation, leading to enhanced arterial inow into the corpus cavernosum, followed by compression of venous channels to maintain erection. This neurovascular process requires
integration with sexual perception and desire. Many drugs
(e.g. prostaglandin E1 analogues and α-adrenergic antagonists) that target this smooth muscle relaxation pathway have
been successfully used in the treatment of ED [12, 13].
Vascular causes of ED, including internal pudendal artery
stenosis, microangiopathy within the corpora cavernosa and
veno-occlusive dysfunction (failure of veins to fully close
during erection), are the focus of potential endovascular
interventions.
32.3.5 Clinical Presentation andEvaluation
• Up to 70% of ED cases remain undiagnosed and untreated.
• ED is associated with high risk for cardiovascular disease,
and the risk equals or exceeds that associated with family
history of myocardial infarction, smoking and hyperlipidaemia. This indicates that all patients presenting with
ED warrant screening for heart disease.
• AUA guidelines emphasize obtaining a thorough medical,
sexual and psychosocial history as the initial step for evaluation. Physical examination typically proves sufcient
for a reliable diagnosis. The International Index of Erectile
Function Questionnaire (IIEF-5) provides a validated
means of ascertaining the symptom severity [14].
32.3.6 Imaging
While penile vascular reconstruction or endovascular angioplasty of internal pudendal or penile arteries can occasionally promote improved erectile function, widespread use of
these techniques in patients with ED. Rigorous trials are
required to demonstrate their short- and long-term efcacy
[15–17]. Initial diagnostic workup consists of:
• Duplex Sonography: Provides pulsed Doppler analysis,
often alongside dynamic erection studies utilizing vasoactive agents. Should USG indicate a possible vascular
cause, the following may be considered [18].
• Cavernosography: Evaluates venoocclusive
dysfunction.
• Internal Pudendal Angiography: For identifying and
potentially treating arterial causes.
32.3.7 Relevant Anatomy
32.3.7.1 Arterial Anatomy (Table32.4)
• Internal Pudendal Artery: Originates from the anterior
division of internal iliac artery, curving under the sciatic
notch facilitating easy identication [19]. It traverses the
perineum along the ischiorectal fossa wall within the
Alcock’s canal.
• Key Branches of the Internal Pudendal Artery:
– Bulbar Artery: Supplies the urethral bulb, posterior
corpus cavernosum and bulbourethral glands.
– Deep Artery of the Penis (Cavernosal Artery): The
primary supply to the erectile tissue of the corpus cavernosum. Divides into helicine arteries entering the
lacunar spaces.
– Dorsal Artery of the Penis: Supplies the glans penis
and prepuce. Lies outside the tunica albuginea, a key
landmark for interventional radiologists.
• Important Anatomical Variation: An accessory puden-
dal artery, often replacing the dorsal penile artery.
32.3.7.2 Venous Anatomy
The penile venous network divides into three layers:
406
Table 32.4 Arterial supply of penis
Artery Description Relevance to erection
Internal pudendal artery Main artery supplying the penis Provides blood ow crucial for erection
Cavernosal arteries Supply the corpus cavernosum Directly responsible for erectile tissue engorgement
Helicine arteries Branches from cavernosal arteries Open into lacunar spaces for erection
S. P. Singh et al.
• Supercial: The supercial dorsal vein drains into the
external pudendal vein and subsequently the great saphenous vein.
• Intermediate: Situated between the tunica albuginea and
Buck’s fascia, this layer is crucial for interventional
radiologists:
– Deep Dorsal Vein: A midline structure running
directly under Buck’s fascia.
– Para-arterial Veins: Typically, four in number, these
drain into the periprostatic plexus.
• Profound:
– Cavernosal Veins: Drain into the periprostatic plexus.
– Urethral Veins: Drain into the internal pudendal vein.
Key Points for Interventional Radiologists
• Understanding the relationships between the dorsal artery
of the penis, the deep dorsal vein and the paired cavernosal veins is essential for precise vascular intervention.
• Awareness of the accessory pudendal artery variation will
aid in procedural planning and troubleshooting.
32.3.8 Penile Doppler
B mode USG is done rst for identifying plaques, brosis,
structural abnormalities and uid collections. A highfrequency linear array transducer (7.5–12MHz) is used.
Pharmacologic induction of an erection is essential for
dynamic vascular assessment. Prostaglandin E1 (10–20μg)
is the most commonly used vasoactive agent and is injected
into the cavernosa. Spectral Doppler of the cavernosal arteries is performed at regular intervals (e.g. every 5minutes)
until maximal peak systolic velocity (PSV) and minimal
end-diastolic velocity (EDV) values are achieved.
Diagnostic Criteria and Interpretation of Doppler
Waveforms
• PSV≥30cm/s generally indicates normal arterial function. PSV < 25 cm/s is diagnostic of arterial
insufciency.
• EDV<5cm/s suggests competent venoocclusive mechanisms. EDV>5cm/s, in the presence of normal arterial
function, indicates venous leakage.
• Resistive index (RI)= (PSV − EDV)/ PSV. RI > 0.8 is
considered normal.
32.3.9 Cavernosometry andCavernosography
Indications
Evaluation of suspected venous leakage contributing to erectile dysfunction in patients without major penile arterial
abnormalities. Provides insights into venoocclusive
dysfunction.
Equipment
• 19-gauge buttery needles (x2)
• Nonionic, low-osmolar, water-soluble contrast
• Heparinized saline
• Pressure-monitoring equipment
Technical Aspects
1. Needle Placement: Buttery needles into each corpus
cavernosum at the mid-shaft, targeting the space between
the dorsal and ventral surfaces. Blood reux conrms
positioning. Avoid local anaesthesia to preserve neuro-
logic response.
2. Infusion: Begin contrast infusion (contrast diluted 1:4in
heparinized saline, maximum 450ml total) under pressure at a rate of approximately 40 ml/min. Continuous
uoroscopy should visualize:
– Filling of the contralateral corpus cavernosum (fenes-
trated septum).
– Filling of supercial and deep penile-draining veins.
– Filling of glans penis (corpus spongiosum) in some
patients.
3. Monitoring: Track intracavernous pressure via the second needle. Target infusion volume sufcient to produce
tumescence/erection is typically 80–120 mL. Normal
subjects should achieve intracavernous pressure of
80mmHg or higher.
4. Post-procedure: Disconnect the needles. Consider aspiration to clear contrast and apply a compressive dressing
to mitigate hematoma risk.
Interpretation
• Venous leakage is demonstrated by the lack of a robust
erection response despite contrast infusion and with minimal intracavernous pressure increase. Prostatic (Santorini)
plexus rapidly lls in these cases [20].
32 Endovascular Interventions forMale Infertility
407
32.3.10 Dynamic Infusion Cavernosometry
andCavernosography (DICC)
DICC expands the diagnostic capabilities by including [18]:
• Phase 1: Intracavernosal injection of a vasoactive agent
to induce pharmacologic erection.
• Phase 2: Venoocclusive function testing to assess how
effectively the corpora increase venous outow
resistance.
• Phase 3: Measurement of systolic occlusion pressures
within left and right cavernosal arteries.
• Cavernosography: Performed as the DICC’s nal
component.
Complications
• Cavernosography is generally considered safe with mini-
mal complication risk. The most frequent issues are:
– Small hematoma formation at the puncture site.
– Potential discomfort related to uid administration.
• Severe complications, including priapism or cavernosa
thrombosis, are extremely rare.
Outcomes
• Cavernosometry-guided cavernosography has established
diagnostic utility in conrming venous leakage as a cause
of ED and to guide interventions such as [20]:
– Surgical techniques aimed at addressing venous leak
– Sclerotherapy or vasoactive drug administration
32.4 Endovascular Treatment ofHigh-
Flow/Non-ischaemic/Arterial Priapism
(Fig.32.1)
32.4.1 Indications
• Conrmed diagnosis of high-ow priapism based on clinical assessment, penile blood gas analysis or Doppler USG.
• Failure of conservative management.
Patient Presents with Priapism
Assess duration, pain level, potential trauma history
Suspect High-Flow Type?
Doppler Ultrasound and/or Pelvic Angiography
Selective Embolization of Fistula
Resolution of Priapism?
Ye sNo
NoYe s
Manage as low-flow
Fig. 32.1 Management of high-ow priapism
Re-evaluate embolization site, consider repeat procedureMonitor recovery, assess erectile function over time
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32.4.2 Contraindications
• No specic contraindications typically preclude this
intervention.
32.4.3 Equipment
• Standard angiographic setup including 5F access sheath.
• Catheters: Pigtail or Cobra-2 5 F (for internal iliac),
Roberts uterine artery catheter is also suitable.
• 0.035-inch angled Glidewire
• 2.7F microcatheter
• Intra-arterial nitroglycerin (10μg/mL)
• Non-ionic contrast (iodine, 300mg/mL)
• Embolic Agents:
– Hand-cut gelfoam pledgets
– 2–3mm diameter microcoils
32.4.4 Technical Aspects
• Fistula Localization: Pre-procedural duplex USG or CT
is ideal to pinpoint the stula side, minimizing the risk of
ED from bilateral embolization [21]. In the absence of
pre-procedural imaging, a pelvic angiogram can identify
the bleed site.
• Selective Catheterization: Catheterize both external and
internal pudendal arteries. Microcatheters facilitate this,
deep internal iliac catheterization is unnecessary.
• Vasodilation: Intra-arterial nitroglycerin (10-μg aliquots)
enhances angiographic visualization.
• Targeted Embolization: Aim for precise placement in
the minor arterial branches near the stula. This approach
protects cavernosal blood supply and potentially preserves erectile function. Microcoils or small gelfoam
pledgets are both accepted embolic agents. Insert each
gelfoam pledget followed by immediate angiography to
conrm positioning. For large stulas, microcoils
(2–3mm) may be used alone or in combination with gelfoam, though these might be palpable to the patient
post-procedure.
• Bilateral Embolization: Rarely necessary, even with
bilateral stulas [22, 23]. It is typically reserved for cases
where unilateral embolization proves ineffective.
• Take great care to avoid non-target embolization. Note
that normal bulbar spongiosa capillary blush might
mimic a bleed site but will not persist into the venous
phase.
32.4.5 Procedure Timing
• Although a few cases of high-ow priapism resolve spontaneously, irreversible endothelial changes and risk of ED
increase with long-standing priapism. Early embolization
(preferably within a few weeks of diagnosis) often yields
better outcomes [22, 23].
32.4.6 Outcomes
• Angiographic conrmation of success should be evident
immediately [24].
• Resolution of priapism (corpora cavernosa detumescence): expected within 24 hours, often sooner
(4–6hours). Recurrence within the rst 24hours is most
likely.
• Failure of resolution after 24hours requires duplex ultrasound or repeat angiography to evaluate for embolization
failure.
• Incidence of ED: Low (3%–9%) following successful
embolization [24].
32.4.7 Complications
• Pudendal artery spasm is likely if antispasmodic agents
are not used during the procedure.
• ED—in case of embolization of the penile artery.
32.4.8 Post-Procedural Care
• Fistula recanalization occurs in 10%–30% of cases and
warrants repeat embolization. This occurs more frequently with gelfoam than coils [25].
• Erectile function typically recovers within weeks to several months. Many cases of bilateral embolization have
been documented to have maintained erectile function.
32.5 Internal Pudendal Angiography
andAngioplasty inErectile
Dysfunction
32.5.1 Indications
• Suspected vascular cause of ED, particularly after abnormal ndings on Doppler studies [26].
32 Endovascular Interventions forMale Infertility
409
32.5.2 Contraindications
• Absolute: ED primarily driven by conrmed psychogenic, neurogenic, or hormonal factors [15, 16].
• Relative: Absence of prior duplex USG and presence of
nocturnal penile tumescence.
32.5.3 Equipment
• Standard angiographic setup (include 5F access sheath,
long hydrophilic 6F sheaths)
• Catheters: Cobra-2 5F (internal iliac) or Roberts uterine
artery catheter
• Wires: Angled 0.035-inch Glidewire and torquable 0.018inch wires
• Intracorporal papaverine (30–60mg), intra-arterial nitroglycerin (50–200μg)
• Non-ionic contrast (iodine, 300mg/mL)
• Angioplasty balloons sized between 2 and 5mm diameter
32.5.4 Technical Aspects
1. Vasodilation: Induce erection via intracorporal papaver-
ine injection (30–60mg) to maximize arterial inow and
minimize venous outow prior to angiography.
2. Intra-arterial Injections: During imaging, a combination
of nitroglycerin (50–200 μg) and papaverine (30 mg)
intra-arterially enhances the angiographic assessment.
3. Selective Angiography: Target anterior division of the
internal iliac artery (6 mL injection at 3 mL/min).
Ipsilateral oblique (35°) with caudal-cranial angulation
(−10°) facilitates the best internal pudendal visualization
and accessory vessel identication.
4. Intervention:
– Standard angioplasty techniques are used for common
iliac stenoses.
– Torquable 0.018-inch guidewires are often necessary.
– Balloon size selection: Proximal lesions generally
need 3–5mm, distal lesions 2–3mm.
– Intravenous heparin (5000–10,000U) as the guidewire
crosses the stenosis.
• Patient selection is the key: Rigorous diagnostic ltering
impacts angiographic ndings and potential for successful intervention.
• Studies on efcacy of angioplasty for ED are limited and
report highly variable success rates (12.5%–100%). This
likely stems from poor initial patient assessment, failure
to exclude small penile vessel stenoses and venoocclusive
ED missed upon imaging [18].
32.5.6 Complications
• Risks standard to any angioplasty/endovascular procedure apply.
32.5.7 Post-Procedure andFollow-Up
• Antiplatelet Therapy: Initiate before the procedure (aspirin 100mg/day, clopidogrel 75mg/day), at least two days
prior. Continue double platelet inhibition for three
months, and lifelong aspirin is likely advisable.
• Management of Comorbidities: Emphasize lifestyle
changes and pharmacotherapy targeting the risk
factors.
• Outcome Assessment: IIEF-5 questionnaires pre- and
post-intervention allow objective outcome tracking.
• Failed Improvement: Warrants cavernosography/cavernosometry, especially in those cases where initial imaging was less comprehensive. Distal vessel disease
inaccessible to angioplasty might be amenable to surgical options.
32.6 Retrograde Venous Occlusion
inVenous Leak Erectile Dysfunction
32.6.1 Indications
• Documented venous leak as the primary ED causes via
DICC assessment [27].
• Retrograde catheterization offers access to a wider range
of potential leakage sites compared to surgery.
32.5.5 Outcomes
• Lesion location patterns help inform aetiology [18]:
– 31–44% of cases: iliac or internal pudendal arteries.
– 29–58% of cases: lesions at the penile base.
– Younger patients commonly exhibit cavernosal artery
disease (62%).
32.6.2 Contraindications
• Absolute: Psychogenic, neurogenic or hormonal causes
of ED not fully excluded [27, 28].
• Absence of conrmed venous leakage on Doppler or prior
cavernosography.
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S. P. Singh et al.
32.6.3 Equipment
• Venous Access: Long hydrophilic sheath via jugular vein
often provides superior ease in targeting internal pudendal veins compared to a femoral approach. Otherwise,
standard angiographic tools apply.
• Sclerosing Agents:
– 1% Aethoxysklerol (laureth-9, polidocanol)
– Lipiodol/N-butyl cyanoacrylate (1:1 ratio).
32.6.4 Procedural Planning
• Combined Cavernosography: Signicantly enhances
the procedure by pinpointing leak sites and providing a
real-time roadmap for retrograde guidance, minimizing
contrast usage.
• Alternative Access Option: Forgoing cavernosography
is possible via direct catheterization of the deep dorsal
penile vein.
32.6.5 Technical Aspects
• Leak Site Targeting: Utilize either the cavernosography
roadmap or, if performed separately, carefully visualize
leak points during the retrograde venogram.
• Sclerotherapy:
– Inject sclerosant in small volumes while the patient
performs a Valsalva manoeuvre to prevent distal ow
of the embolising agent.
– Goal: Occlude major sites of leak into the periprostatic
plexus and pudendal veins. A part of the venous outow must be preserved.
32.6.6 Outcomes
• Complete resolution of ED is uncommon. Although
improvement rates reach up to 69%, recurrence is a concern [27–29].
32.6.7 Complications
32.6.8 Post-Procedure andFollow-Up
• Outcome Assessment: Baseline and post-treatment
IIEF-5 questionnaires aid in objective tracking.
• Doppler Validation: Penile duplex ultrasound can con-
rm intervention success.
• Treatment Failure: Options for patients whose venous
leak does not respond to intervention include surgical
repair or penile prosthetic implantation.
32.7 Conclusion
Interventional radiology plays an important role in the management of both high-ow priapism and erectile dysfunction. Super-selective embolization is a minimally invasive
treatment option for high-ow priapism with reduced risk of
future problems with erection. While the use of endovascular
interventions for erectile dysfunction remains controversial,
careful patient selection and a thorough vascular workup,
utilizing imaging modalities like duplex USG, cavernosography and arteriography, can help identify a sub-group of
patients who may benet from targeted angioplasty or retrograde venous occlusion techniques. Ongoing research and
validation of outcomes will further clarify the scope and
potential benets of interventional radiology procedures in
andrology.
High-Flow Priapism
1. Super-selective embolization is the treatment of choice
for high-ow priapism.
2. Early intervention is critical. Addressing high-ow pri-
apism within a few weeks of diagnosis leads to better outcomes and reduced risk of erectile dysfunction.
3. Precise stula localization is the key. Pre-procedural
imaging allows for the identication of the stulas, minimizing unnecessary treatment and reducing the risk of
complications.
4. Microcoils and gelfoam are the preferred embolic
agents. The choice of material may depend on stula size
and operator experience.
5. Post-procedure erectile dysfunction rates are low.
Successful embolization typically preserves erectile function with relatively low risk.
• Inadvertent distal embolization is a potential concern.
While repeat venous embolization can be done, complete
penile venous outow blockage carries a risk of ischaemia and gangrene.
Erectile Dysfunction
6. Patient selection is important for effective intervention. Endovascular treatment of erectile dysfunction
(ED) remains controversial due to a lack of rigorous