1. Presenter – Dr. Sumit S. Hadgaonkar
Moderator – Dr. Ak. Kaku Singh
2. Definition
A pathological condition of penile erection
characterized as prolonged and devoid of sexual
stimulation or excitement.
Persistent painful purposeless (uncontrolled) erection
of the penis (or clitoris)
> 4hours
Corpora cavernosa only
all age groups (including newborns)
usually pain (except in non-ischaemic type)
3. Priapos (Priapus) was the
Greek God of fertility who is
usually pictured with a
massive erection.
This painting was
discovered in the wall of a
temple in Pompeii, destroyed
by the eruption of Mount
Vesuvius in 79 AD. It shows
Priapos “weighing his
erection.”
4. Epidemology
Occurrence although deemed infrequent is
measurable
Internationally: no information available
Intracaverous injection therapy led to rise in no. of
cases
Sickle cell disease (SCD) most common cause in
pediatric age group
29 % - 45 % life time probability for SCD for
development of priapism
5. Demographics
Race - no predilection (although sickle cell disease, of
course, is a condition of the African American
population)
Sex - disease of males. Clitoral priapism has been
described rarely
Age - all ages, but peak in sickle cell patients between
19 & 21 years
9. Physiology
Penile erection generated by
sensory stimulation of genitalia
spinal reflex arc - reflexogenic erection
afferent from penis through pudendal nerve to sacral spinal
erection center (S2-S3-S4)
efferent parasympathetic fibers travel back in Nervi erigentes
and stimulate blood vessels of corpora cavernosa
sympathetic fibers in thoracolumbar erection center (T12-L1)
innervate vas deferens
10. Physiology
Penile erection generated by
psychogenic stimuli from higher brain centers
descend through lateral
columns and stimulate
thoracolumbar and
sacral spinal erection
centers
11. Physiology
Nitric oxide - an endogenous vasodilator - is released from
nerve endings and endothelial cells and binds to receptors on
smooth muscle of corpora cavernosa
Cyclic guanosine monophosphate (cGMP) is formed,
relaxing smooth muscle and allowing engorgement
Phosphodiesterase type 5 (PDE5) catalyzes cGMP to GMP,
leading to reversal of the above process
Sildenafil (Viagra®), a recently released drug for erectile
dysfunction, acts as a PDE5 inhibitor, helping to maintain a
physiologic erection
12. Pathophysiology
Persistent erection of corpora cavernosa due to
disturbances in detumescence mechanisms - i.e.
inflow >> outflow
Corpora spongiosum of the glans and peri-urethral
region unaffected
Arterial high-flow - usually due to rupture of
cavernous artery and unregulated flow into lacunar
spaces - NOT generally painful
Veno-occlusive (low-flow) - full and unremitting
corporeal veno-occlusion
13. Mortality and Morbidity
Deaths have been reported in patients with sickle cell
disease and priapism, but due to complications from
underlying disease process
Main morbidity is long-term impotence, especially
when diagnosis and treatment are delayed
14. Etiology
Hematological dyscrasias
1.SCD
2.Other hemoglobinopathies
3.Leukamia – Chr. Granulocytic variant
4.asplenisa
5.Fabry’s disease
Thrombotic risk
1.erythropetin use
2.hemodialysis (even with heparin)
3.cessation of oral warfarin
4.TPN (containing 20% fat emulsion)
15. Contd..
Non hematological malignancies
1. Ca penis, urethra ,bladder ,prostate, kidney
2.rectosigmoid carcinoma
Neurological conditions
1.lumbar disk prolapse
2.spinal cord injury
3.lumbar canal stenosis
4.cauda equina compression from metastases
5.anaesthesia – both GA and SA
16. Contd…
Trauma ( presentation is delayed)
1. direct penile or perineal trauma
2.traumatic needle insertion for intracavernous
injection
Erectile dysfunction therapy
1. Intracavernous injections
2.intra urethral alprostadil
3.sildenafil
17. Contd..
Other drugs
1.Antihypertensives – hydralazine ,alpha blockers
2.antipsychotics and antidepressants – SSRIs,
phenothiazines etc.
3.Heavy alcohol intake
4. Immunosuppressants - tacrolimus
5.Androgen supplements
6. Scorpion toxins
Idiopathic – account for 50% off the total cases
24. Classification
Low flow or Ischaemic (veno-occlusive)
most common
Painful sec to tissue ischemia and smooth muscle
hypoxia (compartment syndrome)
Nonischaemic (arterial)
less common
up regulated cavernous inflow
usually not fully erect and painless
25. Low-flow priapism
Low flow or Ischemic (veno-occlusive)
most common
Penis fully erect (sludging of blood within)
Painful sec to tissue ischemia and smooth muscle
hypoxia (compartment syndrome)
blood gases from corpora – acidosis,
hypoxia,hypercapnia
NO & prostacyclin
platelet aggregation and adhesion - thrombus formation
and tissue damage
Increased risk of fibrosis, irreversible cavernous tissue
damage and erectile function loss
Causes ---most off them earlier noted
Emergency management required
26. High-flow priapism
Nonischaemic (arterial)
less common
Penile, perineal or pelvic trauma
uncontrolled arterial inflow directly into the penile
sinusoidal spaces
usually penis not fully erect and painless
often prolonged history
normal local blood gases
no risk of ischemia and subsequent fibrosis
28. Priapism variants
Stuttering priapism
-recurring episodes
-associated with SCD
- every episode same as low flow or ischemic
Refractory priapism
-non ischemic priapism after treatment for ischemic
variety
Neurogenic priapism
-defect in neuroregulation of erection
-it may be central or periphera
Drug induced
-both ischemic and non ischemic type of priapism
produced
29. Diagnosis
History and physical examination
-history should address pain ,duration, prior episodes,
prior clinical treatment ,erectile status prior to attack
-inspection and palpation of penis and abdomen.
- involvement of all 3 structures i.e. glans ,
spongiosm, cavernosa
30. Lab work up
CBC – for hematological abnormalities
Retic count and electrophoresis – for SCD and other
hemoglobinopathies
Urine toxicology – for psychoactive drug abuse
Other routine investigations
31. Penile diagnostics
Aspirate from cavernosum tested for ABG
Color Duplex ultrasound – can be used as an
alternative to aspiration and ABG
Ultrasound – should be done in lithotomy position
and should start with perineum first and then entire
penile shaft
- can diagnose anatomical abnormalities
associated with non ischemic variety
Penile arteriography- mainly used for therapeutic
purpose
32. Treatment
Differ according to type
Based on diagnostic findings
Stepwise approch applied based on
1.reversibility
2. invasiveness
Treatment of historical interest
1.medical -hot water bath 2. surgical-
- ice packs -penile nerve
-enemas transaction
- sedatives -dorsal artery
- leeches ligation
33. Treatment of Ischemic Priapism
Aspiration of cavernous blood
Treatment of related systemic condition
Surgical treatment
Penile prosthesis
34. Aspiration of cavernous blood
Decompression by aspirating cavernous blood with or
without saline irrigation – first line treatment
Scalp vein needle 19-21 G directly inserted into
cavernosum
Saline irrigation with intracavernous phenylephrine
improves results
Done after dorsal penile or penile shaft block
Transglanular intracavernous needle insertion better than
laterally placed needle
35.
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39. Treatment of related systemic
condition
For those priapism associated with known systemic
cause
e.g. Priapism in SCD patients should be managed in
line of sickle cell crisis by hydration, oxygenation,
alkalinization,analgesia.
40. Surgical treatment
For priapism beyond 48-72 hrs
Surgical shunt – to drain blood from cavernosa bypassing
veno-occlusive mechanism
Shunts –
1.Distal cavernoglanular shunts–
a) Winter shunt : large biopsy needle through glans to
cavernosa
b)Ebbehoj shunt : scalpel though glans to cavernosa
c) El –Ghorab shunt :excision of tunica albugenia at tip
of cavernosum
41. Proximal shunts –
a)Quackels / Sacher Shunt : creation of window
between cavernosum and spongiosum
b) Grayhack shunt : saphenous vein anastomosed with
one of the cavernosa
Shunts close after some time hence no permanent
erectile dysfunction (ED) noted .
Shunt complications : 1.urethral fistula
2.purulent cavernositis
3.pulm. embolism (Grayhack)
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45. Penile prosthesis
Significantly delayed presentations that predictably
resulting in erectile dysfunction
Early prosthesis placement recommended
Fibrosis complicates treatment on a later date
46. Treatment of non-ischemic
priapism
Observation –spontaneous resolution in 62% cases
- even duration even in years dose not
affect the outcome
Selective arterial embolisation – for patients desirous
of immediate solution
- both permanent and temporary materials can
be used
- temporary used (for ED prevention)
Exploration and direct surgical ligation of sinusoidal
fistulas or pseudoaneurysms
-50% ED rate
47. Treatment of Stuttering priapism
Treatment of all episodes in line of ischemic priapism
Preventive strategy :
1.Hormonal agents- most efficacy
2.self injection of phenylephrine
3.baclofen
4.digoxin
5.terbutaline
48. Miscellaneous medical treatment
Hydroxyurea – for SCD
TPA/ streptokinase – for ischemic
Methylene blue – for high flow priapism
49. Priapism - complications
Impotence: about 50% incidence
Younger patients seem to do better
Fibrosis: related to tissue ischemia
Makes prosthesis placement difficult
Gangrene: due to ischemia and infection
Suprapubic catheter may help avoid
