quick guide to priapism..

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

6. Anatomy

7. Anatomy

8. Anatomy

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

18. SCD

19. CLL

20. Caverject® self-injection
Urethral
suppository

21. Vacuum pumps and
other “sexual aids”

22. Phoneutria nigriventer - "armed spider"

23. Priapism caused by Phoneutria bite

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

27. Fractured penis

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

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)

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

50. Fournier’s gangrene

52. THANK
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