discussing management of erectile dysfunction

1. Discuss management of
erectile dysfunction.
Urology unit presentation:
Dr Usman Haruna Kamba.
9/11/2012.

2. Outline.
• Introduction
• Definition.
• Relevant anatomy
• Mechanism of erection
• Aetiology of ED
• Classification of ED
• Management of ED
History
Examination.
Investigations
Treatment and complications
• Conclusion
• References

3. Introduction.
• Erectile dysfunction (ED) is persistent or repeated inability, for at least
3 months duration. to auain and/or maintain an erection sufficient for
satisfactory sexual performance.
• common in the elderly
• it may occur even in young adults.
• may involve inadequacy of erection or problems with emission,
ejaculation, or orgasm.

4. • Premature (rapid) ejaculation refers to persistent or recurrent
occurrence of ejaculation with minimal sexual stimulation before, on,
or shortly after penetration and before the person wishes it.
• Retarded ejaculation is undue delay in reaching a climax during sexual
activity.
• Retrograde ejaculation denotes backflow of semen into the bladder
during ejaculation owing to an incompetent bladder neck mechanism.

5. • Anorgasmia is the inability to achieve an orgasm during conscious
sexual activity, although nocturnal emission may occur.

6. • The penile erection is dependent upon corpora cavernosa and
arteriolar smooth muscle relaxation as well as increase venous
outflow resistance.
• The process is initiated by psychic and erotic stimuli from the brain or
tactile stimuli from the genitalia through afferents in the pudenda!
nerve to the spinal cord ($2.,3,4).

7. Innervation of the penis

8. Arterial supply.
• The paired internal pudendal artery is the major carrier of the blood
supply to the penis, dividing into three branches:
• Bulbourethral artery: -supplies the corpus spongiosum
• Dorsal artery: - the skin, subcutaneous tissue, and the glans penis;
• Cavernous artery (deep artery). - supplies the corpora cavernosa.

9. Venous drainage.
• The venous drainage of the glans is mainly through the deep dorsal vein.
• The corpus spongiosum is drained via the circumflex, urethral, and bulbar
veins,
• the corpora cavernosa is more complex:
• mid- and distal shaft : - drained by the deep dorsal and periarterial veins
to the preprostatic plexus.
• the proximal portion is drained by the cavernous and crural veins to the
preprostatic plexus and internal pudendal vein.
• The drainage of all three corpora originates in the subtunical venules,
which unite to form emissary veins

10. Venous drainage.
• The glans penis possesses numerous large and small veins that
communicate freely with the dorsal veins.
• The penile skin and subcutaneous tissue are drained by superficial
dorsal veins, which then empty into the saphenous veins.

12. Mechanism of Penile Erection
• The penile erectile tissues, involved in erection process are:
• Corpora cavernosa.
• Arteriolar, and arterial wall smooth musculature.
• Flaccid state: the smooth muscles contracts due to intrinsic smooth-muscle
tone and tonic adrenergic discharge, allowing only a small amount of
arterial flow for nutrition.
• PO2 is about 35 mm Hg.
• When smooth muscles relax due to the release of neurotransmitters,
resistance to incoming flow drops to a minimum.
• Arterial and arteriolar vasodilatation, and sinusoids expand to receive a
large increase of flow.

13. Mechanism of Penile Erection
• Trapped blood causes penis to lengthen and widen rapidly until the
capacity of the tunica albuginea is reached.
• Also, stretching of the layers of the tunica albuginea compresses the
emissary veins and effectively reduces the venous flow to a minimum.
• Increase in Intracavernous pressure (ICP) and PO2 increase to about
100 and 90 mm Hg, respectively, raises the penis from a dependent
position to the erect state;
• Contraction of the ischiocavernosus muscles result in the rigid-
erection phase

14. Phases of the erection process.
• Flaccid phase (1)
• Minimal arterial and venous flow;
blood gas values equal those of
venous blood.
• Latent (filling) phase (2)
• Increased flow in the internal
pudendal artery.
• Decreased pressure in the internal
pudendal artery;
• unchanged intracavernous pressure.
Some elongation ofthe penis.
• Tumescent phase (3)
• Rising intracavernous pressure until
full erection is achieved.
• Penis shows more expansion and
elongation with pulsation.
• The arterial flow decreases as the
pressure rises.
• When intracavernous pressure rises
above diastolic pressure, flow occurs
only in the systolic phases.

15. Phases of the erection process.
• Full erection phase (4)
• Intracavernous pressure can rise to
as much as 90–100% of the systolic
pressure.
• Arterial flow is less than that in the
initial filling phase but is still higher
than in the flaccid phase.
• The total venous flow is slightly
higher than venous flow in the
flaccid phase.
• Blood gas values approach those
of arterial blood.
• Rigid erection phase (5)
• As a result of contraction of the
ischiocavernous muscle, the
intracavernous pressure rises well
above the systolic pressure,
resulting in rigid erection.
• During this phase, no blood enters
the corpus cavernosum.
• The duration of this phase is short
and does not cause ischemia or
tissue damage

16. Phases of the erection process.
• Detumescent phase (6)
• After ejaculation or cessation of
erotic stimuli, sympathetic tonic
discharge resumes, resulting in
contraction of the smooth
muscles around the sinusoids
and arterioles.
• This diminishes the arterial flow
to flaccid level, reopens the
venous channels, and expels
blood from the sinusoidal
spaces.
• The penis returns to its flaccid
length and girth.

18. AETIOLOGY OF E.D
Psychogenic Erectile Dysfunction
• Psychogenic ED frequently coexists with other sexual dysfunctions,
notably reduced libido and with major psychiatric disorders
particularly depression and anxiety

19. AETIOLOGY OF E.D
• Organic Erectile Dysfunction
Arterial Causes
• Arterial insufficiency is a major factor in pathogenesis of organic ED. The
arteriopathy usually develops secondary to:
1. diabetes mellitus (DM),
2. hypertension,
3. hyperlipidaemia,
4. smoking, lack of exercise,
5. obesity or metabolic syndrome.
6. Rarely posttraumatic arterial obliteration or fistula can also lead to ED.

20. AETIOLOGY OF E.D
• Venous Causes
• In the rigid phase of erection, the venous outflow from the penis is shut off
by nervous stimulation and kinking of the veins as they pass through the
tunica albuginea.
• Failure of this venous outflow causes a venous leak, leading to ED.
Common causes of a venous leak are
• Primary large venous leak draining the corpora cavernosa.
• Traumatic injury to tunica albuginea (e.g. penile fracture).
• Acquired shunt (e.g. after operative intervention for priapism).
• Degenerative changes associated with old age, DM, and Pyronie disease.

21. AETIOLOGY OF E.D
Neurological Causes
• Disruption of the erectogenic neural pathways (central and peripheral)
leads to the development of ED.
• Causes of Central Neuropathy are:
• Multiple sclerosis (MS)
• Cerebrovascular accidents
• Malignancy (e.g. brain and spinal cord)
• Parkinson disease
• Multisystem atrophy
• Spinal cord transection

22. AETIOLOGY OF E.D
Causes of Peripheral Neuropathy:
• MS
• DM
• Sacral cord injury and pelvic fracture
• Radical pelvic surgery
Hormonal Causes
• Hyperprolactinaemia causing ED is found in about 5% of men. .
• Hyper‐ or hypothyroidism,
• Cushing disease, and hypogonadism.

23. AETIOLOGY OF E.D
• Drugs
• Antihypertensives (e.g. beta‐blockers, angiotensin‐converting enzyme
[ACE] inhibitors), diuretics (e.g. thiazides), amiodarone,
• Antidepressants (e.g. tricyclic antidepressants, monoamine oxidase
inhibitors, and serotonin reuptake inhibitors).
• Finasteride, cyproterone acetate, luteinising hormone releasing
hormone (LHRH) analogues.
• Anticonvulsants (e.g. phenytoin, carbamazepine),
• Anti‐Parkinson drugs (i.e. levodopa).

24. MANAGEMENT OF E.D
• A detailed medical, sexual, and psychosocial history.
• Physical examination
are the most important steps in the differential diagnosis of sexual
dysfunction.

25. HISTORY
Onset of symptoms,
early morning erection, loss of libido, and ejaculatory disorders to establish the
type of ED (psychogenic or organic).
Patients detail past medical history of
• DM
• hypertension
• cardiovascular diseases, neurological diseases, pain or angulation of penis,
• History of trauma or pelvic surgery,
• Drug history;
• History of smoking,
• Alcohol intake, or substance misuse .

26. HISTORY
• Any previous treatment for ED and the response
• Validated ED questionnaires such as the International Index of Erectile
Function (IIEF) is useful to record objective evidence of severity of ED

27. Physical examination: general, abdominal,
neurological, and cardiovascular examinations.
• Blood pressure and signs of
arteriopathy.
• Body mass index (BMI) and waist
circumference.
• Secondary sexual characteristics.
• Genital examination (i.e. note size of
penis and testes, presence of penile
plaque or angulation, phimosis, or
hypospadias).
• Evidence of previous trauma or pelvic
surgery.
• Penile sensation.
• Bulbocavernosus reflex (i.e. squeezing
the glans leads to contraction of the
anal sphincter and Bulbocavernosal
muscles; this tests the integrity of S2–
4).
• Testicular examination: size, location,
abnormality, or abscess.
• Digital rectal examination (DRE):
perineal sensation,
• anal reflex or tone, and prostate
examination

28. INVESTIGATIONS.
• FBS
• FBC
• E/U/CR
• LIPID PROFILE
• HORMONAL PROFILE
• PSA
• TFT

29. SPECIALISED TESTS
• Penile dopler USS
• Penile arteriography. For trauma related ED or pt considered for
vascular surgery
• Carvernosography to determine venous leak.
• Nocturnal penile detumescence and rigidity testing for psychogenic
E.D

30. Treatment.
• General measures:
• Identify any reversible cause of ED (e.g. drug induced or hormonal
abnormalities).
• Correction of underlying disorder (e.g. good glycaemic control,
correction of hyperlipidaemia, hyperprolactinaemia, cessation of
smoking, weight loss, and exercise).
• Lifestyle changes and risk factor modification (e.g. exercise, weight
reduction, and avoidance of precipitating factors)

31. Treatment.
• All patients with significant cardiovascular disease need to see a
cardiologist before ED treatment
• Psychosexual therapy for patients with psychiatric disorders and
younger patients with ED.

32. Treatment.
• First‐Line Medical Therapy
• Phosphodiesterase 5 inhibitors
• Three phosphodiesterase 5 (PDE5) inhibitors are approved by for
treatment of ED.
• However, these agents cannot initiate erection, and hence, require
sexual arousal to facilitate erection.

33. Treatment.
• Mechanism of Action
• In the smooth muscle lining (of the trabecular network of
• the cavernosal tissue) of the penis, PDE5 enzyme hydrolyses cyclic
guanosine monophosphate (cGMP) to 5 cGMP.
• PDE5 inhibitors prevent this hydrolysis, and hence, results in
prolonged smooth muscle relaxation, increased arterial flow, and
penile erection.

34. Treatment.
• Second‐Line Therapy
Intracavernosal Injections
• Alprostadil, a synthetic PGE1, is used as a second‐line agent for
treatment of ED.
• It results in corporal and glandular smooth muscle relaxation by
increasing cyclic adenosine monophosphate (cAMP)

35. Treatment.
• Alprostadil is the only drug approved for intracavernous treatment of
ED.
• Usually, the starting dose is 5 μg, but can be increased up to 20 μg.
The needle is inserted into the corpus cavernosum on the lateral aspect
of the mid‐penile shaft at a 90º angle.
• The erection appears after 5–15 minutes and lasts according to the
dose injected.
• Efficacy is reported in >70% of patients with ED.

36. Treatment.
Adverse Effects
• Penile pain (50%).
• Prolonged erections (5%).
• Fibrosis (2%).
• Priapism (1%).
Contraindications
• History of hypersensitivity to Alprostadil.
• Men at risk of priapism.
• Bleeding disorders (Sickle Cell disease

37. Treatment.
Intra‐urethral Alprostadil
• A specific formulation of Alprostadil in a medicated pellet (medicated
urethral system for erection [MUSE]) is approved for use in ED.
• The dose ranges from 125 to 1000 μg.
• With intra‐urethral Alprostadil, erections sufficient for intercourse are
achieved in 30–70% of patients.
Adverse Effects
• Local pain (35%).
• Dizziness with possible hypotension (1.9–14%).

38. • Urethral bleeding (5%).
• Penile fibrosis and priapism (<1%).
• Urinary tract infections (0.2%).

39. Treatment.
• Vacuum Erection Device
Principle
• A vacuum erection device VED consists of three components: a
vacuum chamber, pump, and a constriction band.
• It provides passive engorgement of the corpora cavernosa, together
with a constrictor ring placed at the base of the penis to retain blood
within the corpora.
• Satisfaction rates range between 27 and 94%.

40. Treatment.
• Adverse Effects
• Penile pain.
• Inability to ejaculate.
• Petechiae or bruising.
• Penile numbness.
• Skin necrosis (can be avoided if patients remove the constriction ring
within 30 minutes).

41. Treatment.
• Third‐line Therapy: Penile Prostheses
• It may be considered in patients who do not respond to
pharmacotherapy or who prefer a permanent solution to their
problem.
• The two currently available classes of penile implants are:
• Inflatable (two and three piece).
• Semi‐rigid.
• Malleable devices.

42. Treatment.
• Prosthesis implantation has one of the highest satisfaction rates (92–
100% in patients and 91–95% in partners)
• Patients must be warned that they will have a floppy glans and will
need exchanging of the device after 10 years.
• complications:
• Infection (5%).
• Erosion (5%).
• Mechanical failure (4%).

43. Treatment.

44. INDICATION SURGERY
• Members of the Erectile Dysfunction Guideline Update Panel
provided a definition of the Arterial Occlusive Disease Index patient.
• The panel assumed that the patient who is likely to benefit from
arterial reconstructive surgery is an otherwise;
• healthy man,
• 55 years old or younger,
• recently acquired ED due to focal arterial occlusive disease.
• Absence of other risk factors such as smoking or diabetes to
eliminate patients with either diffuse vascular disease or cavernous
myopathy due to chronic ischemia

45. • Anaesthesia/Preoperative antibiotics
• Position
• Routine cleaning /draping
• Choice of instrument/loops/sutures
• Adequate lightening
• Inscission

46. Surgical Technique
• From a technical standpoint, the operation is divided into
• three stages:
• Dorsal artery dissection,
• IEA harvesting, and donor vessel transfer
• Microsurgical anastomosis.
Dorsal Artery Dissection
• In this stage, a 5 cm semilunar scrotal incision 2 cm below the
penoscrotal junction is made in the side opposite to the planned
abdominal incision for IEA harvesting.

47. • With the penis stretched, finger blunt dissection along Buck’s fascia
toward the glands allows for inversion of the penis.
• The fundiform ligament is identified and preserved to minimize penile
shortening.
• The selected dorsal artery is isolated and mobilized proximally,
avoiding injury of the dorsal nerves.
• Temporary scrotal closure is performed with staples.

48. Harvesting of the Inferior Epigastric Artery:
• In this stage, a 5 cm transverse incision about three-fourths of the distance
between the umbilicus and the pubis is created with a scalpel.
• Dissection is carried down through Scarpa’s fascia using the bovie cautery, the
rectus fascia is divided vertically, and the rectus muscle is mobilized medially.
• The IEA is identified and mobilized from its origin at the level of the common
external iliac artery to the umbilicus.
• If arterial branches are found, they are controlled with bipolar cautery and
divided.
• During the mobilization of the IEA, papaverine is utilized to prevent vasospasm.
• The distal end of the IEA is clipped near the umbilicus and divided.

49. • Donor Vessel Transfer:
• The scrotal staples are removed and a clamp is utilized to transfer the
IEA to the dorsal aspect of the penis through the external inguinal
ring, which previously was dilated bluntly.
• The abdomen is closed in a multilayer fashion using a running
technique with 0 polyglycolic acid suture for the rectus fascia, 2-0 for
Scarpa’s fascia, and a 4-0 Monocryl (Ethicon) for the skin.

50. Microvascular Anastomosis:
• The penis is reinverted and the operating microscope brought to the
surgical field.
• A Scott retractor is utilized to accommodate the penis for microsurgery.
• The DPA is mobilized and divided in a proximal location on the penile
shaft.
• The proximal end is cauterized using the bipolar.
• Aneurysmal clips are place on the dorsal artery and IEA.
• The adventitia of the distal end of the IEA and proximal dorsal artery is
sharply excised with micro scissors to prevent thrombosis of the
anastomosis.

51. • A microsurgical anastomosis is per formed using a simple interrupted
technique with 10-0 nylon stitches.
• The dorsal aneurysmal clip is removed and back blood flow is
observed documenting anastomotic patency.
• The IEA aneurysmal clip is removed and if there is no anastomotic
leak, the penis is placed back in its normal anatomical position, the
dartos muscle is closed with a running 2-0 polyglycolic acid suture
and the skin with a 4-0 polyglycolic acid suture.
• Patency of the anastomosis is further confirmed by Doppler
ultrasound.

52. • Contraindications:
• Contraindications for penile revascularization surgery include advanced
age,
• presence of vascular risk factors,
• evidence of neurologic ED,
• untreated hormonal abnormalities,
• active psychiatric disorders,
• evidence of Peyronie’s disease,
• untreated premature ejaculation, and evidence of corporo-occlusive
dysfunction.

53. Post op management
• Ivf
• Antibiotics
• Analgesics
• DVT prophylaxis

54. Conclusion.
• Erectile dysfunction is a common urologic condition
• It constitute significant urologic consultations due to psychosocial
disturbances and relation to infertility
• Management is tasking and costly to both doctors, patients and the
family
• Therefore accurate diagnoses and appropriate treatment and
counselling is of paramount importance.

55. References.
• Tom FL. Male sexual dysfunction: In: Jack WM, Tom FL. editors. Smith
and Tanagho’s General urology. 18th edition. New York:McGraw Hill
Medical: 2016. P596-614.