The sexual history should include information about previous and current sexual relationships, onset, severity and duration of the erectile problem, and previous consultations and treatments. A detailed description should be made of the rigidity and duration of both sexually stimulated and morning erections and of problems with arousal, ejaculation, and orgasm [15]. Assessment of other areas of sexual dysfunction such as ejaculation, libido, and orgasm should be included in the history. Several patient questionnaires have been developed for assessment of ED, including the Sexual Health Inventory for Men (SHIM) and the International Index of Erectile Function (IIEF) [15]. Either of these questionnaires may be used as an adjunct to diagnosis of ED.

Patients with ED should be screened for symptoms of possible hypogonadism, including decreased energy, libido, and fatigue, as well as for symptomatic lower urinary tract infections. Any history of heart disease, hypertension, diabetes mellitus, neurologic disorders, and renal disease should be reviewed. Lifestyle factors that include smoking, obesity, high-fat diet, use of recreational drugs and alcohol, and lack of exercise may be contributing factors. Mental health history and current psychological status are important considerations as depression is a common comorbidity in ED. Medications, including antihypertensive, cardiac, psychotropic, and hypoglycemic agents, are often associated with ED. It may be difficult, however, to separate the medication from the underlying disease as the causative agent of the ED. History of cancer of the pelvic organs, testes, prostate, central nervous system, and spinal tumors and associated treatments including surgery and radiation may contribute to ED.

The physical examination should be focused on the genitourinary, endocrine, vascular, and neurological systems. The exam may reveal unsuspected diagnoses, such as Peyronie’s disease (an acquired, localized fibrotic disorder of the tunica albuginea resulting in penile deformity, mass, and/or pain), or hypogonadism. Signs of hypogonadism include decreased volume and/or turgor of the testes, alterations in secondary sexual characteristics, and gynecomastia. Blood pressure and femoral and peripheral pulses can reflect vascular health. A thorough neurological exam, including visual fields, should be assessed for symptoms of pituitary tumors.

Laboratory testing should be tailored to the patient’s complaints and risk factors. Testing may include fasting glucose or HbA1c, urinalysis, blood chemistry panel, and lipid profile. ED may be an early manifestation of coronary artery disease [16]. Concern for associated cardiovascular disease may warrant further investigation and/or referral to a cardiologist. Hormonal tests include a morning sample for a total testosterone. However, the threshold of testosterone to maintain erectile function is low, and ED is usually a symptom of more severe cases of hypogonadism. Additional hormonal tests, such as prolactin and luteinizing hormone, are performed when low testosterone levels are detected. If any abnormality is observed, referral to an endocrinologist may be indicated.

While most patients with ED can be diagnosed with a thorough history and physical exam, some patients may need referral to a urologist for specific diagnostic tests. These may include nocturnal penile tumescence and rigidity test, intracavernosal injection test, duplex ultrasound of the penis, arteriography, and dynamic infusion cavernosometry or cavernosography.

The etiology and pathophysiology of PE are unknown. A significant proportion of men with ED also experience PE, and it can be difficult to distinguish between them. Other potential risk factors for PE include a genetic predisposition, poor overall health status and obesity, prostate inflammation, thyroid hormone disorders, emotional problems and stress, and traumatic sexual experiences [16].

The diagnosis of PE is based on the patient’s medical and sexual history. Important criteria include whether PE is situational, such as with a specific partner or certain circumstances, and lifelong or acquired and impact on sexual activity and quality of life for both the patient and partner. Physical exam may assist in identifying associated underlying conditions, such as endocrinopathies and urological disorders.

There are several patient questionnaires for use in diagnosing PE. The most commonly used is the Premature Ejaculation Diagnostic Tool (PEDT) [21].

Treatment approaches may include behavioral modification therapies and/or psychotherapy, decrease in sensory input, or controlled use of medications that have delayed ejaculation as part of their side effect profile. Although not approved by the FDA for this indication, oral antidepressants (SSRIs) and topical anesthetic agents have been shown to delay ejaculation in men with PE and have minimal side effects when used for the treatment of PE. Treatment with oral antidepressants should be started at the lowest possible dose that is compatible with a reasonable chance of success. In patients with concomitant PE and ED, the ED should be treated first [20]. Regular follow-up is important to evaluate efficacy and side effects. Support and education of the patient and, when possible, the partner are an integral part of PE therapy [20].

The majority of patients who report inhibited ejaculation have no clear etiology. There is an association with reports of personal or relationship distress and general health issues [15]. Any medical disease, drug, or surgical procedure that interferes with either central (including spinal or supraspinal) control of ejaculation or the autonomic innervation to the seminal tract, including the sympathetic innervation to the seminal vesicles, the prostatic urethra, and the bladder neck, or sensory innervation to the anatomical structures involved in the ejaculation process, can result in delayed ejaculation, anejaculation, and anorgasmia [23]. Specific causes of delayed or absent ejaculation include medications, sympathetic denervation, hormone deficiency, lower urinary tract infections, and spinal cord injury.

Treatments include psychosexual counseling, medication therapy or discontinuation of interfering medication, hormone replacement, and vibratory stimulation.

Retrograde ejaculation results from damage to the sympathetic innervation of the ejaculatory system and bladder neck. RE may be caused by anatomic abnormalities such as urethral strictures, bladder neck resection, or fibrosis. Neurologic causes include multiple sclerosis, spinal cord injury, retroperitoneal lymphadenectomy, prostate or colorectal surgery, or diabetic neuropathy. Pharmacologic agents can also result in RE, primarily antihypertensive drugs, alpha-adrenergic blocking drugs, antipsychotics, and antidepressants [15].

Patients with absent or low-volume ejaculate should be tested using semen analysis and urinalysis. Diagnosis is confirmed by the presence of sperm in a post-ejaculation urine sample. Diagnosis may result following evaluation for infertility due to azoospermia.

In cases of pharmacologic etiology, discontinuation of the medication may resolve the problem. Pharmacotherapy is most often used for neurologic causes, particularly if partial nerve damage exists. Current drugs include alpha-adrenergic agents such as ephedrine, or tricyclic antidepressants with anticholinergic effects. Successful response is most likely found in patients with partial nerve damage.