Contributors of Campbell-Walsh-Wein, 12th edition
Alan W. Shindel, Tom F. Lue, Arthur L. Burnett Ii, Ranjith Ramasamy, Gregory A. Broderick, Chris G. Mcmahon, Matthew J. Mellon, John J. Mulcahy, Allen D. Seftel, Hailiu Yang, Ervin Kocjancic, Valerio Iacovelli, and Omer Acar
Erectile dysfunction
Epidemiology
Erectile dysfunction (ED) is the inability to attain and/or maintain penile erection sufficient for sexual performance or satisfaction. ED affects up to 20% of men worldwide older than 20 years old and worsens with age. Prevalence begins at 1%–10% for men younger than 40 years and approaches 50%–100% for men older than 70 years. Medical comorbidities, such as metabolic syndrome and cardiovascular disease, are associated with ED. Lower education and cigarette smoking are additional predictors for developing ED. The inverse is also true, and ED is now considered a sentinel for future risk of cardiovascular disease. The major risk factors for ED are in Table 14.1 .
| CONDITION | MULTIVARIATE ADJUSTED ODDS RATIO |
|---|---|
| Diabetes mellitus | 2.9 |
| Hypertension | 1.6 |
| Cardiovascular disease | 1.1 |
| Hypercholesterolemia | 1.0 |
| Benign prostate enlargement | 1.6 |
| Obstructive urinary symptoms | 2.2 |
| Increased body mass index (>30 kg/m 2 ) | 1.5 |
| Physical inactivity | 1.5 |
| Current cigarette smoking | 1.6 |
| Antidepressant use | 9.1 |
| Antihypertensive use | 4.0 |
Pathophysiology
ED and can be broadly separated into psychogenic and organic etiologies ( Box 14.1 ), with most having a functional organic disorder. Organic causes include vasculogenic (most common), neurogenic, anatomic, and endocrinologic. The metabolic syndrome and its components cause impaired penile perfusion secondary to generalized atherosclerosis, subsequent increased vascular resistance, vascular tone, and fibrosis. These, in turn, lead to a decline in erectile function.
Organic
- I.
Vasculogenic
- A.
Arteriogenic
- B.
Cavernosal
- C.
Mixed
- A.
- II.
Neurogenic
- III.
Anatomic
- IV.
Endocrinologic
- V.
Medication induced
Psychogenic
- I.
Generalized
- A.
Generalized unresponsiveness
- 1.
Primary lack of sexual arousability
- 2.
Aging-related decline in sexual arousability
- 1.
- B.
Generalized inhibition
- 1.
Chronic disorder of sexual intimacy
- 1.
- A.
- II.
Situational
- A.
Partner related
- 1.
Lack of arousability in specific relationship
- 2.
Lack of arousability because of sexual object preference
- 3.
High central inhibition because of partner conflict or threat
- 1.
- B.
Performance related
- 1.
Associated with other sexual dysfunction (e.g., rapid ejaculation)
- 2.
Situational performance anxiety (e.g., fear of failure)
- 1.
- C.
Psychological distress or adjustment related
- 1.
Associated with negative mood state (e.g., depression) or major life stress (e.g., death of partner)
- 1.
- A.
ED can also be secondary to neuronal dysfunction. Because erection is a neurovascular event, any disorder of the brain, spinal cord, or peripheral nerves can negatively impact erectile function. Similarly, iatrogenic damage to the cavernosal nerves and vasculature after radical pelvic surgery or after pelvic fracture may cause ED. Damage to the peripheral nervous system from diabetes mellitus can decrease erectile function. Endocrine disorders such as low serum testosterone, as well as hyperprolactinemia, hyperthyroidism, and hypothyroidism, levels often lead to decreases in erectile function and libido.
Last, ED can be drug induced. Many antihypertensive medications can lead to reversible ED, as seen in Table 14.2 . Other drug classes correlated with ED include antipsychotics, antidepressants, recreational drugs, and more. Table 14.3 summarizes many of these medications and suggests possible alternatives.
| AGENT | EFFECT | MECHANISM |
|---|---|---|
| Diuretics | ED (twice as common as placebo) | Unknown |
| β-Blocker (nonselective) | ED | Prejunctional α 2 -receptor inhibition |
| α 1 -Blocker | Decreases ED rate but may cause alteration of ejaculation | Failure of sympathetic-induced (1) closure of internal sphincter and proximal urethra and (2) failure of seminal emission during ejaculation |
| α 2 -Blocker | ED | Inhibition of central α 2 -receptor |
| Angiotensin-converting enzyme inhibitor | Possible reduction in ED | |
| Angiotensin II receptor blocker | Possibly reduction in ED |
| CLASS | KNOWN TO CAUSE ERECTILE DYSFUNCTION | SUGGESTED ALTERNATIVES |
|---|---|---|
| Antihypertensives |
|
|
| Psychotropics |
| Newer anxiolytics (bupropion, buspirone) |
| Antiandrogen |
| N/A |
| 5α-Reductase inhibitors | ||
| Recreational drugs |
|
|
Clinical manifestations
ED manifests with marked difficulty in obtaining erections, maintaining them until completion of sexual activity, and/or a significant decrease in erectile rigidity. Many men have a poor understanding of ED and its symptoms and may confuse ED with decreased libido or disorders of ejaculation.
Diagnosis and testing
The diagnosis of ED differs from most urologic diagnoses in that extensive diagnostic procedures are generally not required. Therefore, the diagnosis can be made based on the patient’s report of consistent inability to attain and/or maintain an erection sufficient for satisfactory sexual intercourse. Several well-validated questionnaires, such as the Index of Erectile Function (IIEF), are useful adjuncts to the patient’s history. The physical exam should focus on the neurologic, cardiovascular, and genital systems. Obvious physical signs of hypogonadism such as small testes or gynecomastia should be noted. ( https://www.auanet.org/guidelines/guidelines/erectile-dysfunction-(ed)-guideline )
Laboratory tests are not mandatory for diagnosis of ED but can help delineate the etiology. Recommended laboratory tests include serum chemistries, fasting glucose or hemoglobin A1c, complete blood count (CBC), lipid profile, and morning serum total testosterone . Further diagnostic testing such as intracavernosal injection of erectogenic medications with or without penile duplex ultrasonography (PDU) are used at the clinician’s discretion to better characterize the arterial or venoocclusive mechanisms of ED.
Treatment
The most recent American Urological Association (AUA) guidelines advocate that all therapeutic options for ED be offered, with any being a valid initial therapy. This demonstrates a shift from the traditional escalation from least to most invasive treatments. An algorithm for ED treatment pathways is seen in Fig. 14.1 .
Lifestyle modification is a primary treatment for ED. Weight loss, diet, exercise, and decrease in cigarette smoking can lead to meaningful improvements in ED. Switching or ceasing a causative medication can lead to significant improvement. The AUA guidelines also propose a referral to a mental health professional to promote treatment adherence, reduce performance anxiety, and integrate treatments into a sexual relationship.
The most common medications for ED are oral phosphodiesterase type 5 inhibitors (PDE5is). These medications augment (but do not induce) the erectile response. Each PDE5i has similar efficacy but different biochemical properties, and several can be used daily or on demand. These medications result in successful sexual intercourse rates of approximately 70% . Success may be lower in patients with DM, previous pelvic surgery, or radiation. Side effects include headache, dyspepsia, flushing, and visual disturbances . Dose titration is recommended. The only true contraindication is coadministration with nitrate-containing medications for angina.
Intracavernosal injection (ICI) of alprostadil, papaverine, phentolamine, or a combination is another highly effective pharmacologic therapy. Because of a higher risk of priapism, it is recommended that the first injection be in clinic and to start with a low dose . ICI is contraindicated in men with psychological instability, coagulopathy, unstable cardiovascular disease, reduced manual dexterity, and concurrent use of monoamine oxidase inhibitors. Alprostadil can also be administered as an intraurethral suppository (IUS), albeit with lower success rates (~50%). It is thus often used in combination with PDE5i. IUS should also be tested in the office to avoid the rare case of hypotension. Vacuum erection devices can be an effective alternate but are often considered cumbersome by patients.
In patients with subnormal testosterone values who are considering ED treatment with PDE5is, they can be counseled that testosterone replacement therapy (TRT) can improve the efficacy of PDE5i but should not be used as monotherapy.
One of the most effective methods of ED treatment is the surgical placement of a penile prosthesis. Inflatable penile prostheses (IPPs) are more popular than a malleable variant. IPPs have high patient and partner satisfaction because they can be utilized on demand for as long and as frequently as desired. On the other hand, implantation is associated with the inherent risks of surgery and leads to irreversible ED if removed. Device failure is rare. Loss of penile length is a common complaint but, if present, is minimal. Patients should be extensively counseled about this risk preoperatively.
Many emerging therapies, such as extracorporeal shock wave therapy, ICI of stem cells, and platelet-rich plasma injections, have shown promising preliminary results. However, due to lack of quality data, they are still considered investigational in the 2018 AUA ED guidelines .
Priapism
Epidemiology
Priapism is defined as an erection that lasts more than 4 hours after sexual stimulation and orgasm. Its incidence in the United States is 5.34 per 100,000 men per year. The most prominent risk factor for developing priapism is sickle cell disease (SCD). The lifetime probability of a man with SCD developing priapism is 29%–42%, or approximately one third of all priapism cases. Potential etiologies are listed in Box 14.2 .
α-Adrenergic receptor antagonists
Prazosin, terazosin, doxazosin, tamsulosin
Antianxiety agent
Hydroxyzine
Anticoagulants
Heparin, warfarin
Antidepressants and antipsychotics
Trazodone, bupropion, fluoxetine, sertraline, lithium, clozapine, risperidone, olanzapine, chlorpromazine, thioridazine, phenothiazines
Antihypertensives
Hydralazine, guanethidine, propranolol
Attention-deficit/hyperactivity disorder agents
Methylphenidates (Concerta, Daytrana, Focalin, Metadate, Methylin, Quillivant, Ritalin)
Atomoxetine (Strattera)
Recreational drugs
Alcohol, cocaine (intranasal and topical), crack cocaine, marijuana, synthetic cannabinoids
Genitourinary conditions
Straddle injury, coital injury, pelvic trauma, kick to penis or perineum, penile bypass surgery, urinary retention
Hematologic dyscrasias
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
Hormones
Gonadotropin-releasing hormone, testosterone
Infectious (toxin-mediated) causes
Scorpion sting, spider bite, rabies, malaria
Metabolic conditions
Amyloidosis, Fabry disease, gout
Neoplastic causes (metastatic or regional infiltration)
Prostate, urethra, testis, bladder, rectum, lung, kidney
Neurogenic conditions
Syphilis, spinal cord injury, cauda equina compression, autonomic neuropathy, lumbar disk herniation, spinal stenosis, cerebral vascular accident, brain tumor, spinal anesthesia, cauda equina syndrome
Vasoactive erectile agents
Papaverine, phentolamine, prostaglandin E 1 , oral phosphodiesterase type 5 inhibitors, combination intracavernous therapy
Pathophysiology
Priapism is typically classified by its etiology: ischemic (low-flow), nonischemic (high-flow), and stuttering. Ischemic priapism accounts for the majority of cases.
Ischemic priapism.
The pathophysiologic process of ischemic priapism begins after an erection persists beyond 4 hours. In SCD, sickled erythrocytes obstruct penile venous outflow, leading to stagnant blood in the corpora cavernosa and ischemia. Several other blood dyscrasias or thrombotic states can lead to ischemic priapism. Rarely, metastases to the penis from other sites can lead to venous outflow obstruction and priapism. Ischemic priapism can also be iatrogenic. Up to 5% of men receiving diagnostic ICI of an erectogenic medication subsequently develop ischemic priapism, which can also happen with home use. Oral (PDE5i) monotherapy, on the other hand, rarely causes priapism.
Nonischemic priapism.
This is usually secondary to blunt or penetrating trauma resulting in laceration of the cavernous artery or one of its penile branches. The most common cause is straddle injury, with trauma during sexual intercourse, kicks to the penis or perineum, and pelvic fracture comprising additional mechanisms. Occasionally, treatment of ischemic priapism with multiple injections, aspiration, or shunts, may lead to rapid conversion to high-flow, non-ischemic priapism.
Stuttering priapism.
This is recurrent priapism that may be associated with stuttering nocturnal or early morning erections, dehydration, fever, and exposure to cold. Patients with SCD may experience this from childhood, and any patient who has experienced ischemic priapism in the past is at increased risk of developing stuttering priapism.
Clinical manifestations
Ischemic and nonischemic priapism differ in their clinical presentation. Patients with ischemic priapism report a fully rigid and painful erection. In nonischemic priapism, the patient is usually less than fully rigid and has a painless erection. In stuttering priapism, patients often awaken with an erection that persists over 4 hours and becomes painful secondary to ischemia. The erection lasts several hours before spontaneous remission. A comparison of the common clinical findings between the types of priapism is in Table 14.4 .
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