Материал: Oxford American Handbook of Urology ( PDFDrive )
492 CHAPTER 12 Erectile function and ejaculation
Retrograde ejaculation
Definition
This is a failure of adequate bladder neck contraction, resulting in the propulsion of sperm back into the bladder on ejaculation.
Etiology
It is secondary to damage or dysfunction of the bladder neck sphincter mechanism.
Underlying causes may be neurological (spinal cord injury; neuropathy associated with diabetes mellitus; nerve damage after retroperitoneal surgery) or anatomical disruption following transurethral resection of ejaculatory ducts (for obstruction), bladder neck incision (BNI), transurethral resection of the prostate (TURP), or open prostatectomy.
It may also occur as a result of selective A-blocker therapy for BPH (particularly tamsulosin).
Incidence
Retrograde ejaculation following TURP or open prostatectomy occurs in 9 out of 10 men and after BNI in 1–5 in 10 men.
Presentation
Dry ejaculation (failure to expel ejaculate fluid from the urethral meatus) and cloudy urine (containing sperm) in the first void after intercourse are the presenting symptoms.
Investigation
The presence of >10–15 sperm per high-powered field in a post-ejac- ulate mid-stream urine specimen confirms the diagnosis of retrograde ejaculation.
Treatment
Medical therapy is initiated in men wishing to preserve fertility and is only effective in patients who have not had bladder neck surgery. Oral adrenergic drugs may be used to increase the sympathetic tone of the bladder neck smooth muscle sphincter mechanism. Drugs include ephedrine sulfate (25–50 mg qid), pseudoephedrine (60 mg qid), or imipramine (25 mg bid).
Therapy is often given for 7–10 days prior to a planned ejaculation (coordinated with the partner’s ovulation). Alternatively, sperm retrieval may be attempted. Oral sodium bicarbonate and adjustment of fluid intake are initiated to optimize urine osmolarity and pH and to enhance sperm survival.
Sperm are collected by gentle urine centrifuge and washed in insemination media in preparation for intrauterine insemination (IUI) or in vitro fertilization (IVF) treatments.
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494 CHAPTER 12 Erectile function and ejaculation
Peyronie’s disease
Definition
This is a benign penile condition characterized by curvature of the penile shaft secondary to the formation of fibrous tissue plaques within the tunica albuginea. It is also called “a disease of aging tissue in a patient with a youthful libido.”
Epidemiology
Prevalence is ~1%, predominantly affecting men aged 40–60 years (average age, 53 years).
Pathophysiology
Scar formation in the tunica albuginea known as plaque is believed to arise as a result of buckling trauma. Dorsal penile plaques are most common (66%).
The corpus cavernosum underlying the lesion cannot lengthen fully on erection, resulting in penile curvature. It may be associated with distal flaccidity or an unstable penis (due to cavernosal fibrosis). The disorder has two phases:
•Active phase (1–6 months): painful erections and changing penile deformity
•Quiescent phase (9–12 months): disease “burns out.” Pain disappears with resolution of inflammation, and there is stabilization of the penile deformity.
Etiology
The exact cause is unknown. It is likely that repeated minor trauma during intercourse causes microvascular injury and bleeding into the tunica, resulting in inflammation and fibrosis (exacerbated by transforming growth factor-B[TGF-B]).
Autoimmune disease processes have also been suggested, and there is a reported familial predisposition.
Presentation
Patients experience pain and curvature of the erect penis. There is a hard area (plaque) on the penis, as well as erectile dysfunction (30–40%) and penile shortening.
Associated disorders
These include Dupuytren’s contractures (40%), plantar fascial contracture, tympanosclerosis, previous trauma, diabetes mellitus, and arterial disease.
Evaluation
A full medical and sexual history is taken. Patient’s photographs of the curvature are useful. Assess the location and size of the plaque (is it tender?).
Color Doppler US is used to assess vascular abnormalities, whereas contrast-enhanced MRI is indicated for complex and extensive cavernosal fibrosis.
PEYRONIE’S DISEASE 495
Management
Early disease with active inflammation (<3 months, penile pain, changing deformity) benefits most from medical therapy. Surgery is indicated for a stable, significant deformity (preventing intercourse).
Concomitant erectile dysfunction can be treated conventionally (oral or intracavernosal medications; vacuum device; penile implant).
Medical treatments
These consist of vitamin E (200 mg tid) for 3 months; tamoxifen (20 mg bid) for 3 months; or colchicine (500 mg tid) for 6 weeks.
Nesbit procedure
The penis is degloved via a circumglandular incision. An artificial erection is induced by intracavernosal saline injection. On the opposite side of maximal deformity, an ellipse is excised (a width of 1 mm is taken for every 10° of penile curvature) and then closed with sutures.
Success rates are 88–94%. Warn the patient that penile shortening of 2–3 cm frequently occurs.
Penile plication
This involves placement of soft permanent sutures in parallel rows along the convex side of the penile shaft. Penile shortening of 0.4–1.5 cm is reported in 40% of patients.
Pain at the site of tunical suture placement is reported in roughly 12%.
Plaque incision and grafting
This involves incision of plaque with venous patch insertion to lengthen the affected side (and minimize penile shortening). Other grafts reported include nonautologous grafts of dermis, porcine small intestinal submucosa (SIS) or pericardium, or autografts of dermis or rectus abdominis fascia.
Success rates are 75–96%.
Adverse effects include erectile dysfunction in 5–12% of patients.
Penile implant
When significant deformity is coupled with resistant or worsening impotence, placement of an inflatable penile prosthesis with intraoperative “molding” of the deformity is an effective way of treating both problems.
496 CHAPTER 12 Erectile function and ejaculation
Priapism
Priapism is prolonged and often painful erection in the absence of a sexual stimulus, lasting >4–6 hours, which predominantly affects the corpus cavernosa.
Epidemiology
It peaks in incidence at ages 5–10 and 20–50 years.
Classification
Low-flow (ischemic) priapism
This is due to veno-occlusion (intracavernosal pressures of 80–120 mmHg). It is more common than high-flow priapism.
It manifests as a painful, rigid erection, with absent or low cavernosal blood flow. Ischemic priapism beyond 4 hours requires emergency intervention.
Blood gas analysis shows hypoxia and acidosis.
High-flow (nonischemic) priapism
This is usually post-traumatic in nature and does not require emergent intervention. It is due to unregulated arterial blood flow, presenting with a semi-rigid, painless erection.
Blood gas analysis shows similar results to arterial blood.
Etiology
Causes are primary (idiopathic) or secondary (see Tables 12.4 and 12.5):
•Intracavernosal injection therapy—PGE1; papaverine
•Drugs—B-blockers; antidepressants; antipsychotics; psychotropics; tranquilizers; anxiolytics; anticoagulants; recreational drugs; alcohol excess; total parenteral nutrition
•Thromboembolic—sickle cell disease (roughly one-third develop stuttering/recurrent priapism); leukemia; thalassemia; fat emboli
•Malignant infiltration of the corpora cavernosa (e.g., advanced bladder cancer)
•Neurogenic—spinal cord lesion; autonomic neuropathy; anesthesia
•Trauma—penile or perineal injury resulting in cavernosal artery laceration or arteriovenous fistula formation
•Infection—malaria; rabies; scorpion sting
Pathophysiology
Priapism lasting for 12 hours causes trabecular interstitial edema, followed by destruction of sinusoidal endothelium and exposure of the basement membrane at 24 hours, and sinusoidal thrombi, smooth muscle cell necrosis, and fibrosis at 48 hours.
Evaluation
•CBC to exclude sickle cell and leukemia.
•Cavernous arterial blood samples to determine the type of priapism (high or low flow). Ischemic priapism is typically associated with a PO2