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Priapism
DR.LEELA KRISHNA
OVERVIEW
■ Definition
■ Types
■ Epidemiology and Pathophysiology
■ Evaluation and Diagnosis
■ Treatment
History
Greek God PRIAPUS-God of fertility
Definition
■ Persistent penile erection that continues hours beyond, or is
unrelated to, sexual stimulation
■ The guideline definition is restricted to only erections of
greater than four hours duration
■ Typically, only the corpora cavernosa are affected
DEFINITION
■ AUA Committee-“Multifactorial entity of genital organ
tumescence or rigidity, that develops and persists in a
pathologically uncontrolled fashion for any duration without
sexual purpose”
Ischemic Priapism (Veno-Occlusive, Low-
Flow)
 Most common, accounting for more than 95% of all cases
 Persistent erection marked by rigidity of the corpora
cavernosa
 Little or no cavernous arterial inflow
 Abnormal cavernous blood gases (hypoxic, hypercarbic and
acidotic)
 Penile pain
 Rigid Erection
 Emergency
Histological Changes
■ 12 hours
– corporal specimens show interstitial edema, progressing to
destruction of sinusoidal endothelium
■ 24 hours
– Exposure of the basement membrane and thrombocyte
adherence
■ 48 hours
– Thrombus can be found in the sinusoidal spaces, and smooth
muscle necrosis
Nonischemic Priapism (Arterial, High-
Flow)
■ Caused by unregulated cavernous arterial inflow
■ Corpora are tumescent but not rigid and the penis is not
painful
■ History of blunt trauma to the penis or an iatrogenic needle
injury is common
■ Arteriolar-sinusoidal fistula
■ Blood gases are not hypoxic or acidotic-non emergent
Stuttering Priapism (Intermittent)
■ Characterized by a pattern of recurrence
■ Recurrent unwanted and painful erections in men with sickle
cell disease (SCD)
■ Patients typically awaken with an erection that persists for
several hours
■ Becomes progressively painful secondary to ischemia
■ Any patient who has experienced ischemic priapism is at risk
for stuttering priapism
Pathophysiology
■ Imbalance of vasoconstrictive and vasorelaxatory
mechanisms predisposing the penis to hypoxia
■ Corporal smooth muscle cells are exposed to hypoxia, α-
adrenergic stimulation fails to induce corporal smooth muscle
contraction
■ Severe anoxia signifcantly impair corporal smooth muscle
contractility & cause significant apoptosis of smooth muscle
cells & ultimately fibrosis of the CC
■ NO imbalance resulting in
– aberrant molecular signaling
– PDE5 dysregulation
– adenosine overproduction
– Reductions in Rho-kinase activity
■ Which translates into enhanced corporal smooth muscle
relaxation and inhibition of vasoconstriction in the penis.
Etiology
 Hematologic
 Sickle cell disease
 Thalassemia
 Granulocytic leukemia
 Myeloid leukemia
 Lymphocytic leukemia
 Multiple myeloma
 Hemoglobin Olmsted variant
 Fat emboli associated with
hyperalimentation
 Hemodialysis
 Glucose-6-phosphate
dehydrogenase deficiency
 Genitourinary
 Straddle injury
 Coital injury
 Pelvic trauma
 Kick to penis or perineum
 Arteriovenous or
arteriocavernous bypass
surgery
 Urinary retention
 Recreational Drugs
 Alcohol, cocaine, crack
cocaine, marijuana
Etiology
 Neurologic
 Syphilis
 Spinal cord injury
 Cauda equina
compression
 Autonomic neuropathy
 Lumbar disk herniation
 Spinal stenosis
 Cerebral vascular
accident
 Brain tumor
 Spinal anesthesia
 Cauda equina syndrome
■ Neoplastic
– Sarcoma
– Secondaries
– Myeloma
– Lymphoma
– Penis, Prostate, urethra,
testis, bladder, rectum,
lung, kidney
Etiology
 HORMONES
 Gonadotropin-releasing
hormone, testosterone
 INFECTIOUS (TOXIN-
MEDIATED) CAUSES
 Scorpion sting, spider
bite, rabies, malaria
Prostatitis, Urethritis,
Mumps, Syphilis
 METABOLIC CONDITIONS
 Amyloidosis, Fabry
disease, gout, Diabetes,
Nephrotic syndrome,
Renal failure,
Haemodialysis
■ ED pharmacotherapy
– Oral sildenafil
– Intraurethral alprostadil
– Intracavernous agents
– Papaverine, phentolamine,
oral phosphodiesterase type
5 inhibitors
Pharmacologic
Causes
■ α-ADRENERGIC
RECEPTOR ANTAGONISTS
– Prazosin, terazosin,
doxazosin, tamsulosin
■ ANTIANXIETY AGENT
– Hydroxyzine
■ ANTICOAGULANTS
– Heparin, warfarin
■ ANTIHYPERTENSIVES
– Hydralazine,
guanethidine, propranolol
■ ANTIDEPRESSANTS AND
ANTIPSYCHOTICS
– Trazodone, bupropion,
fluoxetine, sertraline, lithium,
clozapine, risperidone,
olanzapine, chlorpromazine,
thioridazine, phenothiazines
■ ATTENTION-
DEFICIT/HYPERACTIVITY
DISORDER AGENTS
– Methylphenidates
– Atomoxetine
HISTORY
 Duration of erection
 Degree of pain
 Previous history of priapism and its treatment
 Erectile function status
 Use of drugs : Antihypertensives; anticoagulants; antidepressants and
other psychoactive drugs; alcohol, marijuana, cocaine,cannabis
 Vasoactive agents used for intracavernous injection
 History of trauma- perineal straddle injury
 History of sickle cell disease or other hematologic abnormality
Examination
Ischaemic Nonischaemic
Corpora cavernosa fully rigid
+ --
Penile pain + --
Abnormal cavernous blood gases
+ --
Blood abnormalities and
hematologic malignancy
+ --
Recent intracavernous vasoactive
drug injections
+ --
Chronic, well-tolerated tumescence
without full rigidity
-- +
Perineal trauma
-- +
Piesis Sign
■ In young children with high flow priapism, perineal
compression with the thumb will cause prompt
detumescence, called Piesis sign-confirmatory
Investigations
■ Complete blood count, platelet count,WBC differential
■ Peripheral smear, reticulocyte count
■ Hb electrophoresis
■ Screening for psychoactive drugs and urine toxicology
■ Corporal Blood gas testing
– Differentiates ischemic from nonischemic priapism.
– Aspiration may be both diagnostic and therapeutic.
– Initial penile aspirate will reveal dark deoxygenated blood with a
“crankcase oil” appearance in ischemic priapism
■ Color duplex ultrasonography
■ Penile arteriography
Source PO2(mm hg) PCO2(mm hg) PH
Normal arterial
blood
>90 <40 7.40
Normal venous
blood
40 50 7.35
Ischemic
priapism(first
corporal
aspirate)
<30
HYPOXIA
>60
HYPERCARBIA
<7.25
ACIDOSIS
TYPICAL BLOOD GAS VALUES
USG Imaging
■ Anatomic
abnormalities
Corporal fibrosis- white dots
bilateral cavernous hematomas ( ) at∗
the base of the penis
Color duplex ultrasonography
 Performed in the lithotomy or
frogleg position
 Scanning perineum first and
then along the entire shaft of
the penis
 Screening test for anatomical
abnormalities--cavernous.A
fistula or pseudoaneurysm in
nonischemic priapism
 Examine perineal corpora
cavernosa
Low flow priapism
Color duplex ultrasonography
Arterial-lacunar fistula due to rupture
of the right cavernosal artery
(arrowheads )
High flow priapism
Angiography
■ Adjunctive study
■ Identify site of cavernous
artery fistula (ruptured
helicine artery)
■ Performed as part of an
embolization procedure
arterial-lacunar fistula due to rupture of the
right cavernosal artery (arrowheads)
Differentiating features
High flow Low flow
pO2 >90 mm Hg <30 mm Hg
pCO2 <40 mmHg >>60mmHg
pH >7.4 <7.2
Pain -- +
Pulsation + -
Palpation Elastic Sturdy
Arterial inflow Present Absent
Venous outflow Open Closed
Viscosity low High
Role Of MRI
■ Imaging of a well-established arteriolar-sinusoidal fistula
■ To demonstrate the presence and extent of tissue thrombus
and corporal smooth muscle infarction
■ Imaging of corporal malignancy or metastasis
Differential diagnosis of priapism
Treatment
■ Management of
ischemic episode-
IMMEDIATE
■ > 4 hours –
irrespective of etiology-
Compartment
syndrome
■ Oral agents are not
recommended in the
management of acute
ischemic priapism (>4
hours)
Aspiration
■ Therapeutic- Decompresses
and relieves pain
■ 36% resolution rate
■ Can flush with saline
■ A single, large-bore, 19-
gauge needle inserted at
penoscrotal junction at 3 or 9
o’clock position
■ Repeated until no more dark
blood can be seen coming out
from the corpora
Aspiration with irrigation
■ Alpha adrenergic agent- phenylephrine
■ α1 agonist, 100-200ug every 5-10 min
■ Epinephrine- 10-20ug every 5 to 10 min
■ Transglanular –less hematoma and facilitate blood
drainage after catheter removal
■ Trans corporal-proximally and distally
■ Blood evacuation needed for drug to be effective
■ Resolution-58% with injection, 77% with combined
Drugs
■ Oral sympathomimetic drugs
■ Effectively reverse
prolonged erection (<4
hours) initiated by ICI
therapies
■ Aspiration followed by the
ICI of sympathomimetic
drugs
■ α-adrenergic agent-
Metaraminol
■ Mixed α&βadrenergic
agonists- Etilefrine,
Phenylephrine
&Epinephrine.
■ Pure β agonist-Terbutaline
■ α-adrenergic agent
contract cavernous
smooth muscles, allowing
sinusoidal blood to egress
from subtunical veins
■ β-adrenergic agent relaxes
cavernous smooth muscle
and dilate cavernous
artery & promote
oxygenated blood to enter
cavernous spaces and
washout deoxygenated
blood
Drugs
■ Phenylephrine:100-200
mcg/ml dilution dose
■ Agent of choice
■ Use 1 mL of 200 mcg/mL
solution via intracavernous
injection in 1 hr.10 Doses
■ Erections > 4 hrs and < 12
hrs, cavernous aspiration, &
irrigation with 10 mL of
1:1,000,000 solution of
epinephrine
■ Let’s Stop This “Epi”demic!
Preventing Errors with
Epinephrine
■ Pseudoephedrine :- 60-
120 mg PO may be given
in cases of priapism of
short duration (2-4 h)
■ Terbutaline -5 mg PO,
repeated after 15 min;
0.25-0.5 mg SC
■ Headache, dizziness,
hypertension, reflex
bradycardia, tachycardia,
and irregular cardiac
rhythms
Surgical Shunts
■ Failed intra cavernous treatment
■ Priapism lasting longer than 24 hours was associated with a 90% ED
rate
■ Ischemic priapism >72 hrs duration
■ Cavernous thrombosis is evident and no blood can be aspirated from
the corporal bodies
■ Surgical intervention may be preferable in patients with malignant or
poorly controlled hypertension
■ Objective – Drain blood from cavernosa bypassing veno occlusive
mechanism & reoxygenation of the cavernous smooth muscle
Shunt procedures are divided based on anatomic
location
■ Percutaneous distal shunts—Ebbehoj, Winter, or T shunt –
First because it is technically easier
■ Open distal shunt—Al-Ghorab or corporal snake
■ Combined T shunt and corporal snake maneuver—Zacharakis
■ Open proximal shunt
■ Saphenous vein—Grayhack and colleagues
■ Deep dorsal vein shunt
T shunt
 Less invasive
 Performed with local anesthetic
in ER
 Creates a T-shaped shunt b/w
the CC and glans penis.
 In T shunting a No. 10 blade is
placed vertically through the
glans 4 mm away from the
meatus; blade pierces through
the glans to the CC and is
rotated 90 degrees away from
the urethra and removed
TUNNEL (T)shunt
 Priapism >36 hrs,
bilateral T shunt, with
insertion of 20-Fr
dilators into the fistula
tract and into the CC
down to the crus
 Technique traumatic
and will require GA
Winter shunt
■ Distal corporo glanular
shunt-with biopsy
needle
■ EBBEHOJ shunt-
scalpel used
AL- GHORAB SHUNT
 Distal caverno glanular
shunt
 2cms transverse
Incision over glans
 Distal corpora excised
as vent
 Most effective distal
shunt
 Performed secondarily-
invasive
Corporal Snake Maneuver
■ Modifcation of the Al-Ghorab
shunt
■ Rather than excising a wedge of
tunica and underlying CC
muscle, a 7/8 Hegar dilator is
advanced through each of the
tunica windows proximally
several cms to release blood
and thrombus
Prevention shunt obstruction
■ Compressive penile dressings should be avoided
■ Patient should periodically squeeze and release the distal
penis to “milk” the shunt maintaining patency
■ Anticoagulation
– Preoperative aspirin 325 mg coupled with subcutaneous
heparin 5000 units and post- operative aspirin 81 mg daily
for 2 weeks
Quackels/Sachers shunt
 Proximal corpus
cavernosum to
spongiosum (CC-CS)
shunt
 Trans-scrotal or
transperineal approach
 Openings placed in
staggered fashion
 Unilateral or Bilateral
Vein shunts
GRAY HACK SHUNT- cavernoso
Saphenous shunt
BARRY SHUNT-cavernoso
dorsal vein shunt
Penile Prosthesis
■ Untreated ischemic priapism or priapism refractory to
interventions is severe fibrosis, penile length loss, and
complete ED
■ Small-Carrion penile prosthesis through an infrapubic incision
■ Semirigid implants
■ “EARLY” implantation - two distinct advantages
ALGORITHM
Prolonged Ischemic priapism
■ LUE’S approach: a 3-step duration dependent approach
■ Stage1< 24 h, Evacuation of old blood + diluted α
adrenergic agent;
■ Stage2- 1–2 d, T-shunt
■ Stage3> 3 d, T-shunt + tunnelling
Non ischemic priapism
■ 62%resolve with observation
■ Duration does not affect outcome
■ Selective arterial embolization-75% resolution
– Non permanent material- clot/gel(5%ED)
– Permanent-Coil, PVP, alcohol-(39%ED)
■ Penile exploration + doppler guided ligation- last
resort-63%resolution, 50%ED
ALGORITHM
Hematologic priapism
■ Sickle cell disease- hydration, oxygenation,
and systemic alkalinisation to prevent
further sickling
■ Corporeal aspiration and intracavernous α
agonists should be given as soon as
possible
Stuttering Priapism
■ Single sympathomimetic
intracorporal injection
■ oral and injectable α-adrenergic
agonists
■ Terbutaline
■ Digoxin,
■ Antisickling agent
hydroxycarbamide (hydroxyurea)
■ Estrogens
■ GnRH analogues
■ Antiandrogens, baclofen,
gabapentin, and recently PDE5
inhibitors
■ Etilefrine - 100 mg in 24
hours at bed time
■ Goal of hormonal therapy
in the prevention of
stuttering priapism is to
reduce serum testosterone
to hypogonadal levels or
block testosterone’s
effects on the penis
■ Mean testosterone levels
fall from baseline of 475
ng/dL to 275 ng/dL
Recurrent priapism
■ Treat each episode as for
ischemic cases
■ Prevent recurrence-
– Self injection phenylephrine
– Gonadotrophins-LHRH Agonist
7.5mg/month
– Anti androgens-bicalutamide 50
mg
– Baclofen(20-40mg OD),
digoxin(0.25 mg)
– Terbutaline
Treatment algorithm
■ Primary outcomes:
– resolution of the priapism (flaccid penis for at least 24 hours),
– recurrence of priapism (after 24 hours of flaccidity)
– erectile dysfunction
Future
 Clinical studies of priapism should
 Documentation of pre-priapism erectile function
 Time from onset of priapism to initial treatment and time
to each subsequent treatment
 Measurement of sexual function after resolution using a
standardized instrument for one year
 Using contemporary validated instruments for assessing
quality of life
THANK YOU

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Priapism ppt

  • 2. OVERVIEW ■ Definition ■ Types ■ Epidemiology and Pathophysiology ■ Evaluation and Diagnosis ■ Treatment
  • 4. Definition ■ Persistent penile erection that continues hours beyond, or is unrelated to, sexual stimulation ■ The guideline definition is restricted to only erections of greater than four hours duration ■ Typically, only the corpora cavernosa are affected
  • 5. DEFINITION ■ AUA Committee-“Multifactorial entity of genital organ tumescence or rigidity, that develops and persists in a pathologically uncontrolled fashion for any duration without sexual purpose”
  • 6. Ischemic Priapism (Veno-Occlusive, Low- Flow)  Most common, accounting for more than 95% of all cases  Persistent erection marked by rigidity of the corpora cavernosa  Little or no cavernous arterial inflow  Abnormal cavernous blood gases (hypoxic, hypercarbic and acidotic)  Penile pain  Rigid Erection  Emergency
  • 7. Histological Changes ■ 12 hours – corporal specimens show interstitial edema, progressing to destruction of sinusoidal endothelium ■ 24 hours – Exposure of the basement membrane and thrombocyte adherence ■ 48 hours – Thrombus can be found in the sinusoidal spaces, and smooth muscle necrosis
  • 8. Nonischemic Priapism (Arterial, High- Flow) ■ Caused by unregulated cavernous arterial inflow ■ Corpora are tumescent but not rigid and the penis is not painful ■ History of blunt trauma to the penis or an iatrogenic needle injury is common ■ Arteriolar-sinusoidal fistula ■ Blood gases are not hypoxic or acidotic-non emergent
  • 9. Stuttering Priapism (Intermittent) ■ Characterized by a pattern of recurrence ■ Recurrent unwanted and painful erections in men with sickle cell disease (SCD) ■ Patients typically awaken with an erection that persists for several hours ■ Becomes progressively painful secondary to ischemia ■ Any patient who has experienced ischemic priapism is at risk for stuttering priapism
  • 10. Pathophysiology ■ Imbalance of vasoconstrictive and vasorelaxatory mechanisms predisposing the penis to hypoxia ■ Corporal smooth muscle cells are exposed to hypoxia, α- adrenergic stimulation fails to induce corporal smooth muscle contraction ■ Severe anoxia signifcantly impair corporal smooth muscle contractility & cause significant apoptosis of smooth muscle cells & ultimately fibrosis of the CC
  • 11. ■ NO imbalance resulting in – aberrant molecular signaling – PDE5 dysregulation – adenosine overproduction – Reductions in Rho-kinase activity ■ Which translates into enhanced corporal smooth muscle relaxation and inhibition of vasoconstriction in the penis.
  • 12. Etiology  Hematologic  Sickle cell disease  Thalassemia  Granulocytic leukemia  Myeloid leukemia  Lymphocytic leukemia  Multiple myeloma  Hemoglobin Olmsted variant  Fat emboli associated with hyperalimentation  Hemodialysis  Glucose-6-phosphate dehydrogenase deficiency  Genitourinary  Straddle injury  Coital injury  Pelvic trauma  Kick to penis or perineum  Arteriovenous or arteriocavernous bypass surgery  Urinary retention  Recreational Drugs  Alcohol, cocaine, crack cocaine, marijuana
  • 13. Etiology  Neurologic  Syphilis  Spinal cord injury  Cauda equina compression  Autonomic neuropathy  Lumbar disk herniation  Spinal stenosis  Cerebral vascular accident  Brain tumor  Spinal anesthesia  Cauda equina syndrome ■ Neoplastic – Sarcoma – Secondaries – Myeloma – Lymphoma – Penis, Prostate, urethra, testis, bladder, rectum, lung, kidney
  • 14. Etiology  HORMONES  Gonadotropin-releasing hormone, testosterone  INFECTIOUS (TOXIN- MEDIATED) CAUSES  Scorpion sting, spider bite, rabies, malaria Prostatitis, Urethritis, Mumps, Syphilis  METABOLIC CONDITIONS  Amyloidosis, Fabry disease, gout, Diabetes, Nephrotic syndrome, Renal failure, Haemodialysis ■ ED pharmacotherapy – Oral sildenafil – Intraurethral alprostadil – Intracavernous agents – Papaverine, phentolamine, oral phosphodiesterase type 5 inhibitors
  • 15. Pharmacologic Causes ■ α-ADRENERGIC RECEPTOR ANTAGONISTS – Prazosin, terazosin, doxazosin, tamsulosin ■ ANTIANXIETY AGENT – Hydroxyzine ■ ANTICOAGULANTS – Heparin, warfarin ■ ANTIHYPERTENSIVES – Hydralazine, guanethidine, propranolol ■ ANTIDEPRESSANTS AND ANTIPSYCHOTICS – Trazodone, bupropion, fluoxetine, sertraline, lithium, clozapine, risperidone, olanzapine, chlorpromazine, thioridazine, phenothiazines ■ ATTENTION- DEFICIT/HYPERACTIVITY DISORDER AGENTS – Methylphenidates – Atomoxetine
  • 16. HISTORY  Duration of erection  Degree of pain  Previous history of priapism and its treatment  Erectile function status  Use of drugs : Antihypertensives; anticoagulants; antidepressants and other psychoactive drugs; alcohol, marijuana, cocaine,cannabis  Vasoactive agents used for intracavernous injection  History of trauma- perineal straddle injury  History of sickle cell disease or other hematologic abnormality
  • 17. Examination Ischaemic Nonischaemic Corpora cavernosa fully rigid + -- Penile pain + -- Abnormal cavernous blood gases + -- Blood abnormalities and hematologic malignancy + -- Recent intracavernous vasoactive drug injections + -- Chronic, well-tolerated tumescence without full rigidity -- + Perineal trauma -- +
  • 18. Piesis Sign ■ In young children with high flow priapism, perineal compression with the thumb will cause prompt detumescence, called Piesis sign-confirmatory
  • 19. Investigations ■ Complete blood count, platelet count,WBC differential ■ Peripheral smear, reticulocyte count ■ Hb electrophoresis ■ Screening for psychoactive drugs and urine toxicology ■ Corporal Blood gas testing – Differentiates ischemic from nonischemic priapism. – Aspiration may be both diagnostic and therapeutic. – Initial penile aspirate will reveal dark deoxygenated blood with a “crankcase oil” appearance in ischemic priapism ■ Color duplex ultrasonography ■ Penile arteriography
  • 20. Source PO2(mm hg) PCO2(mm hg) PH Normal arterial blood >90 <40 7.40 Normal venous blood 40 50 7.35 Ischemic priapism(first corporal aspirate) <30 HYPOXIA >60 HYPERCARBIA <7.25 ACIDOSIS TYPICAL BLOOD GAS VALUES
  • 21. USG Imaging ■ Anatomic abnormalities Corporal fibrosis- white dots bilateral cavernous hematomas ( ) at∗ the base of the penis
  • 22. Color duplex ultrasonography  Performed in the lithotomy or frogleg position  Scanning perineum first and then along the entire shaft of the penis  Screening test for anatomical abnormalities--cavernous.A fistula or pseudoaneurysm in nonischemic priapism  Examine perineal corpora cavernosa Low flow priapism
  • 23. Color duplex ultrasonography Arterial-lacunar fistula due to rupture of the right cavernosal artery (arrowheads ) High flow priapism
  • 24. Angiography ■ Adjunctive study ■ Identify site of cavernous artery fistula (ruptured helicine artery) ■ Performed as part of an embolization procedure arterial-lacunar fistula due to rupture of the right cavernosal artery (arrowheads)
  • 25. Differentiating features High flow Low flow pO2 >90 mm Hg <30 mm Hg pCO2 <40 mmHg >>60mmHg pH >7.4 <7.2 Pain -- + Pulsation + - Palpation Elastic Sturdy Arterial inflow Present Absent Venous outflow Open Closed Viscosity low High
  • 26. Role Of MRI ■ Imaging of a well-established arteriolar-sinusoidal fistula ■ To demonstrate the presence and extent of tissue thrombus and corporal smooth muscle infarction ■ Imaging of corporal malignancy or metastasis
  • 28. Treatment ■ Management of ischemic episode- IMMEDIATE ■ > 4 hours – irrespective of etiology- Compartment syndrome ■ Oral agents are not recommended in the management of acute ischemic priapism (>4 hours)
  • 29. Aspiration ■ Therapeutic- Decompresses and relieves pain ■ 36% resolution rate ■ Can flush with saline ■ A single, large-bore, 19- gauge needle inserted at penoscrotal junction at 3 or 9 o’clock position ■ Repeated until no more dark blood can be seen coming out from the corpora
  • 30. Aspiration with irrigation ■ Alpha adrenergic agent- phenylephrine ■ α1 agonist, 100-200ug every 5-10 min ■ Epinephrine- 10-20ug every 5 to 10 min ■ Transglanular –less hematoma and facilitate blood drainage after catheter removal ■ Trans corporal-proximally and distally ■ Blood evacuation needed for drug to be effective ■ Resolution-58% with injection, 77% with combined
  • 31. Drugs ■ Oral sympathomimetic drugs ■ Effectively reverse prolonged erection (<4 hours) initiated by ICI therapies ■ Aspiration followed by the ICI of sympathomimetic drugs ■ α-adrenergic agent- Metaraminol ■ Mixed α&βadrenergic agonists- Etilefrine, Phenylephrine &Epinephrine. ■ Pure β agonist-Terbutaline ■ α-adrenergic agent contract cavernous smooth muscles, allowing sinusoidal blood to egress from subtunical veins ■ β-adrenergic agent relaxes cavernous smooth muscle and dilate cavernous artery & promote oxygenated blood to enter cavernous spaces and washout deoxygenated blood
  • 32. Drugs ■ Phenylephrine:100-200 mcg/ml dilution dose ■ Agent of choice ■ Use 1 mL of 200 mcg/mL solution via intracavernous injection in 1 hr.10 Doses ■ Erections > 4 hrs and < 12 hrs, cavernous aspiration, & irrigation with 10 mL of 1:1,000,000 solution of epinephrine ■ Let’s Stop This “Epi”demic! Preventing Errors with Epinephrine ■ Pseudoephedrine :- 60- 120 mg PO may be given in cases of priapism of short duration (2-4 h) ■ Terbutaline -5 mg PO, repeated after 15 min; 0.25-0.5 mg SC ■ Headache, dizziness, hypertension, reflex bradycardia, tachycardia, and irregular cardiac rhythms
  • 33. Surgical Shunts ■ Failed intra cavernous treatment ■ Priapism lasting longer than 24 hours was associated with a 90% ED rate ■ Ischemic priapism >72 hrs duration ■ Cavernous thrombosis is evident and no blood can be aspirated from the corporal bodies ■ Surgical intervention may be preferable in patients with malignant or poorly controlled hypertension ■ Objective – Drain blood from cavernosa bypassing veno occlusive mechanism & reoxygenation of the cavernous smooth muscle
  • 34. Shunt procedures are divided based on anatomic location ■ Percutaneous distal shunts—Ebbehoj, Winter, or T shunt – First because it is technically easier ■ Open distal shunt—Al-Ghorab or corporal snake ■ Combined T shunt and corporal snake maneuver—Zacharakis ■ Open proximal shunt ■ Saphenous vein—Grayhack and colleagues ■ Deep dorsal vein shunt
  • 35. T shunt  Less invasive  Performed with local anesthetic in ER  Creates a T-shaped shunt b/w the CC and glans penis.  In T shunting a No. 10 blade is placed vertically through the glans 4 mm away from the meatus; blade pierces through the glans to the CC and is rotated 90 degrees away from the urethra and removed
  • 36. TUNNEL (T)shunt  Priapism >36 hrs, bilateral T shunt, with insertion of 20-Fr dilators into the fistula tract and into the CC down to the crus  Technique traumatic and will require GA
  • 37. Winter shunt ■ Distal corporo glanular shunt-with biopsy needle ■ EBBEHOJ shunt- scalpel used
  • 38. AL- GHORAB SHUNT  Distal caverno glanular shunt  2cms transverse Incision over glans  Distal corpora excised as vent  Most effective distal shunt  Performed secondarily- invasive
  • 39. Corporal Snake Maneuver ■ Modifcation of the Al-Ghorab shunt ■ Rather than excising a wedge of tunica and underlying CC muscle, a 7/8 Hegar dilator is advanced through each of the tunica windows proximally several cms to release blood and thrombus
  • 40. Prevention shunt obstruction ■ Compressive penile dressings should be avoided ■ Patient should periodically squeeze and release the distal penis to “milk” the shunt maintaining patency ■ Anticoagulation – Preoperative aspirin 325 mg coupled with subcutaneous heparin 5000 units and post- operative aspirin 81 mg daily for 2 weeks
  • 41. Quackels/Sachers shunt  Proximal corpus cavernosum to spongiosum (CC-CS) shunt  Trans-scrotal or transperineal approach  Openings placed in staggered fashion  Unilateral or Bilateral
  • 42. Vein shunts GRAY HACK SHUNT- cavernoso Saphenous shunt BARRY SHUNT-cavernoso dorsal vein shunt
  • 43. Penile Prosthesis ■ Untreated ischemic priapism or priapism refractory to interventions is severe fibrosis, penile length loss, and complete ED ■ Small-Carrion penile prosthesis through an infrapubic incision ■ Semirigid implants ■ “EARLY” implantation - two distinct advantages
  • 45. Prolonged Ischemic priapism ■ LUE’S approach: a 3-step duration dependent approach ■ Stage1< 24 h, Evacuation of old blood + diluted α adrenergic agent; ■ Stage2- 1–2 d, T-shunt ■ Stage3> 3 d, T-shunt + tunnelling
  • 46. Non ischemic priapism ■ 62%resolve with observation ■ Duration does not affect outcome ■ Selective arterial embolization-75% resolution – Non permanent material- clot/gel(5%ED) – Permanent-Coil, PVP, alcohol-(39%ED) ■ Penile exploration + doppler guided ligation- last resort-63%resolution, 50%ED
  • 48. Hematologic priapism ■ Sickle cell disease- hydration, oxygenation, and systemic alkalinisation to prevent further sickling ■ Corporeal aspiration and intracavernous α agonists should be given as soon as possible
  • 49. Stuttering Priapism ■ Single sympathomimetic intracorporal injection ■ oral and injectable α-adrenergic agonists ■ Terbutaline ■ Digoxin, ■ Antisickling agent hydroxycarbamide (hydroxyurea) ■ Estrogens ■ GnRH analogues ■ Antiandrogens, baclofen, gabapentin, and recently PDE5 inhibitors ■ Etilefrine - 100 mg in 24 hours at bed time ■ Goal of hormonal therapy in the prevention of stuttering priapism is to reduce serum testosterone to hypogonadal levels or block testosterone’s effects on the penis ■ Mean testosterone levels fall from baseline of 475 ng/dL to 275 ng/dL
  • 50. Recurrent priapism ■ Treat each episode as for ischemic cases ■ Prevent recurrence- – Self injection phenylephrine – Gonadotrophins-LHRH Agonist 7.5mg/month – Anti androgens-bicalutamide 50 mg – Baclofen(20-40mg OD), digoxin(0.25 mg) – Terbutaline
  • 52. ■ Primary outcomes: – resolution of the priapism (flaccid penis for at least 24 hours), – recurrence of priapism (after 24 hours of flaccidity) – erectile dysfunction
  • 53. Future  Clinical studies of priapism should  Documentation of pre-priapism erectile function  Time from onset of priapism to initial treatment and time to each subsequent treatment  Measurement of sexual function after resolution using a standardized instrument for one year  Using contemporary validated instruments for assessing quality of life