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DEFINITION

Persistent painful purposeless erection of the penis (or clitoris) more than 6 hours

EPIDIMIOLOGY
 INCIDENCE
Cases per 100,000 person-years.

 AGE
All age groups (including newborns)
Peak incidence 20 to 50yrs.
Younger age group associated with sickle cell disease
Peak incidence in sickle cell patients  between 19 & 21 years.
 SEX
Priapism is a disease of males.
Clitoral priapism has been described rarely

PATHOLOGY
CLASSIFICATION
Low flow or Ischaemic (veno-occlusive)
Most common
Painful sec to tissue ischaemia and smooth muscle hypoxia (compartment syndrome)
Penis fully erect (sludging of blood within)
Blood gases from corpora - acidosis
 NO & prostacyclin
Platelet aggregation and adhesion - thrombus formation and tissue damage

Non ischaemic (arterial)


Less common
Upregulated cavernous inflow
Usually not fully erect and painless
Penile, perineal or pelvic trauma
Uncontrolled arterial inflow directly into the penile sinsoidal spaces
Often prolonged history
Normal local blood gases
No risk of ischaemia and subsequent fibrosis

Priapism Variants

ETIOLOGY
Causes of low-flow priapism
IDIOPATHIC
Most common cause.
Priapism occurring without any discernible cause is considered to be idiopathic.
Some investigators have estimated that this disorder accounts for as many as half of all
documented cases

SECONDARY
 SYSTEMIC
 Blood diseases
 Hyperviscosity syndromes (sickle-cell disease)
Most common cause in children
42% incidence in adults with sickle-cell disease
64% incidence in boys with sickle-cell disease

 Other haemoglobinopathies
 Leukemic disorders
 Thrombophilia
 Multiple myeloma
 Neurological causes
Rare
Lumbar disc lesions, spinal stenosis, seizure disorders, cerebrovascular disease
 Drugs
 Psychotropic drugs
 Phenothiazines
 Butyrophenones
 Hydralazine
 Prazosin, labetolol, phentolamine and other -blockers
 Testosterone
 Metoclopramide
 Calcium-channel blockers
 Anti-coagulants
 Tamoxifen
 Omeprazole
 Hydroxyzine
 Cocaine, marijuana, and ethanol
 Miscellaneous
TPN, amyloid , rabies, appendicitis

 LOCAL
 Intracavernosal pharmacotherapy
21%
E.g. Papaverine and PGE-1 (alprostadil) intracavernosal injection.
extremely low incidence with oral agents

 Post Trauma
Perineum, groin or penis
Usually cause high flow priapism but can cause low flow sec to haematoma
 Solid Tumors
Malignant infiltration of corpora

High-flow priapism
 Trauma
 sickle-cell disease: Very rare
 Fabry`s disease

PATHO-PHYSIOLOGY
- Due to one of the above etiologic factors  disturbances in detumescence mechanisms
(inflow >> outflow) will happened  Persistent erection of corpora cavernosa
- Corpora spongiosum of the glans and peri-urethral region rarely affected
- Recurrent episodes of priapism can result in enlarged penis, fibrotic corpora and ED
COMPLICATION
Untreated priapism leads to corporal fibrosis and impotence
 early complications:
• CVS: Acute hypertension, headache, palpitations, arythmias
• Bleeding, haematoma
• Infection
• Retention
• Urethral injury
 late complications:
 Fibrosis and impotence
Related to type, duration of priapism and aggressiveness of treatment
Incidence: about 50%
Longer duration implies greater risk of impotence
 Low-flow  high incidence of ED if not treated within 12 hours
 High flow  good prognosis (20% rate of ED)
Fibrosis makes prosthesis placement difficult
Gangrene: due to ischemia and infection

DIAGNOSIS

HISTORY
History of disease
Prolonged erection more than 6h without purpose or sexual need which is painful
Pain is more prominent with low flow.

History of etiology
Low flow priapism may give history of ICI, Sickle cell disease, Leukemia….etc
High flow priapism may give history of perineal or pelvic trauma
About 50% of cases has no definite etiology.
History of complication
Which is more common with low flow (veno-occlusive erection).

Clinical history and


Arterial high-flow priapism
may be delayed after acute injury
may be due to vessel spasm, or formation of clot, which is reabsorbed
less tumescent than venous priapism
less painful than venous priapism
good long-term prognosis

Veno-occlusive priapism
painful erection, present for hours to days
ask about
trauma
drugs - therapeutic and illicit
self-injection
sexual stimulation
history of similar or
predisposing factors

drug history
Veno-occlusive low-flow priapism Arterial high-flow priapism
Past history
Pain painful less painful
Tumescent

Prognosis

C/O & HPI


Usually pain (except in non-ischaemic type

PAST H

FAMILY H

EXAMINATION
GENERAL EXAM
Erect or semi-erect penis with a flaccid glans
Search for signs of trauma
Search for other possible
Signs of sludging - florid
Skin, petechiae,
Conjunctival injection

LOCAL EXAM

INVESTIGATION
LABORATORY
 ROUTINE
urinalysis
a complete blood count may help identify a previously undiagnosed leukemia

 SPECIFIC
haemoglobin S to outrule leukaemia
? Local blood gas measurments

IMAGING
radionucleotide scanning - no longer performed
colour doppler ultrasonography

OTHERS

D.D

TREATMENT
Goal is to
Abort the erection, thereby preventing permanent damage to the corpora (ED).
Relieve pain.

TREATMENT MODALITIES
Treat causal factor where identified
principle is to restore arterial inflow and venous outflow

Medical management of low-flow priapism


Aspiration of the corpora with a 21G butterfly needle followed by an injection of
phenylephrine (1 adrenergic agonist) every 5 minutes until detumescence
10mg/ml phenylephrine in 19mls saline
100% effective if within 12 hours

Oral terbutaline (-adrenoceptor agonist) - 5-10mg


At best 36% response
terbutaline 5 mg po repeated in 15 minutes leads to resolution in about 1/3 of patients
intracavernous injection of -adrenergic
phenylephrine 100 to 500 mcg (put 10 mg in 500cc NSS  20 mcg/ml. Inject 10 to
20 cc every 5-10 minutes (maximum - 10 doses)
dorsal nerve block will be helpful
Aspiration and irrigation
for priapism lasting more than 2 hours
discuss with urologist if at all possible
MUST warn patient treatment may result in permanent impotence
conscious sedation may be necessary
Local anesthetic or penile block
Insert 19-g butterfly into engorged corpus cavernosum through the glans into the distal
portion
Milk out old blood
Irrigate with saline
Elastic wrap (Ace®) to flaccid penis

Sickle-cell –
prompt and conservative as it recurs
Hydration, oxygenation, metabolic alkalinization
Aspiration and injection (as above)
Stuttering priapism
Self injection of -adrenergic agent if sexually active (prophylactic digoxin) or oral -
adrenergic agent (Etilefrine)
Antiandrogen if not to suppress nocturnal tumescence
Low-flow due to sickle cell disease
hydration
alkalinization
analgesia
possible exchange transfusion to get Hgb > 10 gm% and HbS <30%
intracorporeal -adrenergic may be necessary

Surgical management of low-flow priapism


Winter procedure using a Trucut needle
create a shunt between glans and corpora cavernosa
Ebbehoi procedure using a pointed scalpel blade

El-Ghourab procedure
excision of a piece of tunica albuginea
30% of above techniques fail

direct cavernosal-spongiosum anastomosis

corpora-saphenous shunt

lower incidence of ED reported with Winter technique

Intracavernosal thrombolytic agents ??

High-flow priapism
Ice pack  arterial spasm
?? spontaneous thrombosis
Most cases require arteriography and embolisation of the internal pudendal artery or a branch
Arterial priapism - 4 options
Mechanical: iced compression
Pharmacologic: -agonists (watch out for systemic blood pressure rise)
Surgical: fistula ligation (usually leads to impotence)
Selective embolization: new procedure with varying degrees of success

TREATMENT STRATEGIES

FOLLOW UP

PROGNOSIS

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