This man’s history is adequate to rule out arterial or venous insufficiency as he can masturbate to produce a rigid, sustainable erection and he responds well to tadalafil. Due to his report of gradual onset, his lack of response to ongoing sexual therapy, and his tremendous anxiety associated with the issue, the decision was made to offer a PCDU to assess for a vascular etiology for his disorder. PCDU revealed normal peak flow bilaterally of 40 cm/sec with no end diastolic flow and 100% rigidity obtained. His erection lasted more than 2 hours and required phenylephrine to resolve the erection.
This is a 17-year-old male with a past medical history of insomnia, anxiety and depression who presents with complaints of gradual onset (2 years ago) of decreased ability to obtain and maintain erections adequate for intercourse. He reports normal nocturnal erections “most days of the week”. He does not masturbate because he feels that masturbation may have desensitized his brain and caused ED; however, he can masturbate and have an erection with normal orgasm/ejaculation. He has had a successful erection and intercourse with a partner, last time 2 weeks ago. He feels that his ED might have been associated with SSRI treatment but noted no improvement after stopping his SSRI. Cialis 5 mg is effective. He reports normal libido “but not where it was”. His testosterone (T) and free T are normal. He is in the care of a sexual therapist and has read extensively on the internet. He takes trazodone nightly for sleep.
Ultrasound with Doppler imaging (ultrasound plus evaluation of blood flow in the arteries and veins) can provide additional information about blood flow of the penis and may help in the evaluation of patients prior to surgical intervention. This study is typically performed after the injection of a chemical that causes the arteries to open up, a vasodilator (prostaglandin E1), into the corpora cavernosa in order to cause dilation of blood vessels and promote blood flow into the penis. The rate of blood flow into the penis can be measured along with an evaluation of problems with compression of the veins.
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All the above subjects were assessed for the prevalence of one or more sexual dysfunction experienced over the past 12 months using a sexual dysfunction checklist (Appendix A) by a trained psychiatrist (BSA). The checklist contains items corresponding to 12 areas of sexual dysfunction described in the Diagnostic Criteria for Research, ICD-10 Classification of Mental and Behavioural Disorders.[15] This was necessary as the SCAN does not contain a detailed assessment for the ICD-10 section on Sexual dysfunction not caused by organic disorder or disease (F52). The disorders specifically tapped by the checklist were aversion towards sex, low sexual desire, difficulty in achieving and in maintaining erection, premature ejaculation, inhibited or delayed ejaculation orgasm with flaccid penis, anorgasmia, pain at the time of coitus, dissatisfaction with frequency of intercourse per week (in the last year and in a representative week 5 years earlier), partner and, own sexual function.
The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels.
If the patient complains of loss of sensation on his penile shaft or glans, it is useful to perform hot and cold perception testing and/or additional vibratory sensory testing with biothesiometer. These are tests that can be performed quickly during the office visit and provide useful information about the function of the dorsal nerve of the penis (Table 3).

This is a 22-year-old man who presents with no medical or surgical history who reports that he has never had a rigid erection in his life. He reports normal libido, penile sensation, orgasm, and ejaculation. The remainder of his history is negative. His physical examination is normal with normal genital exam and secondary sexual characteristics. He reported no significant change in erection with PDE5 inhibitors.
Instead of injecting a medicine, some men insert a suppository of alprostadil into the urethra. A suppository is a solid piece of medicine that you insert into your body where it dissolves. A health care professional will prescribe a prefilled applicator for you to insert the pellet about an inch into your urethra. An erection will begin within 8 to 10 minutes and may last 30 to 60 minutes.
Ultrasound with Doppler imaging (ultrasound plus evaluation of blood flow in the arteries and veins) can provide additional information about blood flow of the penis and may help in the evaluation of patients prior to surgical intervention. This study is typically performed after the injection of a chemical that causes the arteries to open up, a vasodilator (prostaglandin E1), into the corpora cavernosa in order to cause dilation of blood vessels and promote blood flow into the penis. The rate of blood flow into the penis can be measured along with an evaluation of problems with compression of the veins.
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All three of these involve specific bodily systems including the hormones, muscles, blood vessels, nervous system, and emotions. If any of these systems become compromised, it can cause ED. In the case of anxiety and stress, these things can affect the brain’s ability to send the necessary signals to trigger the desired physical response – an erection. Stress and anxiety can also contribute to an ongoing cycle of ED, as mentioned earlier.


People sometimes refer to ED as "impotence," although the two aren't really the same condition. ED is the physical inability to develop or maintain an erection that is rigid enough for sex. Impotence is a broader term. While one cause of it is ED, impotence may also involve a lack of sexual desire, an inability to ejaculate, or problems with orgasm.

The physical examination can reveal clues for physical causes of erectile dysfunction. A doctor will perform an assessment of BMI and waist circumference to evaluate for abdominal obesity. A genital examination is part of the evaluation of erectile dysfunction. The examination will focus on the penis and testes. The doctor will ask you about penile curvature and will examine the penis to see if there are any plaques (hard areas) palpable. The doctor will examine the testes to make sure they are in the proper location in the scrotum and are normal in size. Small testicles, lack of facial hair, and enlarged breasts (gynecomastia) can point to hormonal problems such as hypogonadism with low testosterone levels. A health care provider may check pulses in your groin and feet to determine if there is a suggestion of hardening of the arteries that could also affect the arteries to the penis.

Poor cardiovascular health reduces your body’s ability to deliver blood needed to produce erections. In a study published in 2004, researchers followed male participants for 25 years. The researchers found that heart disease risk factors predicted which men were most at risk of future ED. Numerous studies have strongly tied four major cardiovascular risk factors to ED:

Premature ejaculation was reported by 36 out of 96 (37.5%) subjects, out of which, 27 (28.12%) had complaints of ejaculating within the first minute itself and the rest (9.38%) ejaculated within three minutes of intromission. The next most frequent sexual dysfunction reported was low sexual desire, which was reported by 36 out of 100 subjects. Erectile dysfunction was reported by 33.3% of the subjects with difficulty in achieving erection in 19 subjects (19.79%) and difficulty in maintaining erection in 13 subjects (13.54%).
Ageing is one of the most important unmodifiable risk factors for the development of metabolic disorders and CV diseases. Accordingly, the common algorithms for the estimation of risk of forthcoming diabetes or CV events include age as a factor of the equations (24-29). The weight attributed to age for estimating the risk in these equations is often so significant that younger men are automatically considered at low risk, irrespective of the other possible risk factors. However, even in younger subjects, overlooking the contribution of cardio-metabolic factors to pathogenesis of ED is a mistake that can lead to the loss of the opportunity of early recognition of patients who deserve a change in life-style or a pharmacological correction of risk factors. ED, besides being considered one of the clinical manifestations of metabolic and cardiovascular diseases (CVD), is regarded as an early marker of CV events (17). In fact, according to Montorsi’s hypothesis (30), impairment of penile artery blood flow occurs before that of coronary or carotid arteries, whose diameter is greater and needs longer time to acquire a clinically relevant damage. The clinical consequence of this pathological event is that ED often manifests earlier than myocardial infarction or stroke. In particular, it has been demonstrated that ED occurs on average three years before the first major adverse CV event (MACE) (31). Quite surprisingly, although CV risk increases with ageing, the role of ED as a harbinger of forthcoming MACE becomes progressively less evident. Data derived from almost 2,500 community-dwelling men aged 40–79 years, involved in the Olmsted County study show that ED is associated with an almost 50-fold higher risk of incident heart diseases in men aged 40–49 years, whereas the difference in risk between ED and non-ED men progressively declines in older men (32). The different CV risk associated with ED in different age bands has been confirmed by the meta-analysis of the available longitudinal studies (33). These observations suggest that, in younger men, the role of ED as a marker of CV risk is even more dramatic than in older ones and as a consequence, investigating the presence of metabolic or CV conditions in younger ED patients is pivotal for identifying men in whom an early life-style modification may avoid serious CV consequences. Even more than erection during sexual intercourse, erection during masturbation is considered a physiologic function that mirrors metabolic and CV health. In fact, erections during masturbation are far less affected by relational and psychological components than sex-related ones (34). In a population of subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, more than 2,500 men reported autoeroticism in the previous 3 months. Among these men, the impairment of erection during masturbation was associated with family and personal history of CVD (35), as well as with impaired response to the test with the intracavernous injection (ICI) of prostaglandin E1, which suggests an arteriogenic damage of penile arteries and predicts forthcoming MACE (36). For a subset of these men (n=862), information on the occurrence of MACE during a mean follow-up of 4.3 years was available and those who reported impaired erections during masturbation had a significantly higher incidence of MACE (35). However, when considering separately younger and older men, this association was confirmed only in younger ones, and it was still significant after excluding men reporting severe ED during masturbation (35). This suggests that the impairment of erection during masturbation is a symptom not completely overlapping with sex-related ED and that it can provide different and supplementary information, in particular when assessed in younger and apparently healthy men. Similarly to what is observed for erection during masturbation, acceleration of blood in penile arteries, as measured by the colour Doppler ultrasound in flaccid conditions, is associated with an adverse CV profile in men consulting for ED. A reduction in flaccid acceleration, which can be used by clinicians to objectively verify the arteriogenic origin of ED and to characterize the extent of a self-reported symptom, has been also associated with a future risk of CV events, with the association being significant in younger but not in older men (37).
The lab testing obtained for the evaluation of erectile dysfunction may vary with the information obtained on the health history, physical examination, and recent lab testing. A testosterone level is not necessary in all men; however, a physician will order labs to determine a patient's testosterone level if other signs and symptoms of hypogonadism (low testosterone) such as decreased libido, loss of body hair, muscle loss, breast enlargement, osteoporosis, infertility, and decreased penile/testicular size are present.
And yes, this may all seem easier said than done, when it comes to a condition that is more often than not the subject of jokes—or the cause of embarrassment. Talking to your doctor is the first step in dealing with this complication, which can wreak havoc on your quality of life. Keeping diabetes in check and enjoying a healthy lifestyle can make a huge difference in reducing ED risk, but if that isn't enough, there are successful treatments. Sex brings a range of physical and psychological benefits, whether you have diabetes or not. Preventing or reversing ED isn't just about sex—it's a step toward better health and a more satisfying life.

• Blood Vessels: Diabetes damages blood vessels, especially the smallest blood vessels such as those in the penis. Diabetes can also cause heart disease and other circulatory problems. Proper blood flow is absolutely crucial to achieving erection. “Erection is a hydraulic phenomenon that occurs involuntarily,” says Arturo Rolla, MD, of Harvard University School of Medicine. “Nobody can will an erection!” Anything that limits or impairs blood flow can interfere with the ability to achieve an erection, no matter how strong one’s sexual desire.
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