The vacuum device creates a vacuum to pull blood into the penis. Unlike a normal erection, the inflow of blood does not continue once the individual removes the vacuum device. The rubber band placed at the base of the penis constricts the penis to prevent the blood from leaving the penis. As there is no inflow or outflow of blood when the rubber band is in place, it is uncommon for the tip of the penis (the glans) to appear a little blue and the penis to be cooler. Once intercourse is completed, the individual removes the rubber band and the blood drains out of the penis.
Alcohol abuse is the leading cause of impotence and other disturbances in sexual dysfunction.[3] Episodic erectile failure in alcoholic men is fairly routine, found to be significantly higher in men consuming more than three standard units of alcohol (12 g ethanol) daily and in subjects smoking more than 10 cigarettes/day.[4] Van Thiel and Lester[5] reported that 61% of patients dependent on alcohol reported sexual dysfunction, the most common being erectile dysfunction followed by reduced sexual desire. Erectile dysfunction and reduced sexual desire were frequently seen to be coexisting.[6–9] Vijayasenan,[10] found that of 97 male inpatients admitted for the treatment of alcoholism, 71% suffered from sexual dysfunction for a period of more than 12 months prior to admission to a hospital. The disturbances noted were diminished sexual desire (58%), ejaculatory incompetence (22%), erectile impotence (16%) and premature ejaculation (4%). Virtually all aspects of the human sexual response are affected by alcohol especially sexual desire and erection.[11]
"Sexual relations are not only an important part of people's wellbeing. From a clinical point of view, the inability of some men to perform sexually can also be linked to a range of other health problems, many of which can be debilitating or potentially fatal," says Professor Gary Wittert, Head of the Discipline of Medicine at the University of Adelaide and Director of the University's Freemasons Foundation Centre for Men's Health.
The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
This patient has thoroughly researched erectile dysfunction on the internet and has a powerful knowledge base from which he draws reference. He is also emotionally labile. The most urgent recommendation for this patient is that he seek appropriate psychiatric treatment to help in management of his psychiatric conditions and suicidal ideation. It was also recommended that he seek care with a sexual therapist to work through additional issues related to his “addiction” to masturbation. During his urologic visit we performed both cold and hot perception testing and biothesiometer, which were normal. He was displeased with these findings as they were incongruent with his chief complaints; normal results caused him to become tearful. A penile ultrasound was performed without injection of a pharmacologic agent to assess the appearance of his cavernous tissue and cavernous arteries, which had normal appearance and measurement, respectively, on ultrasound. (This quick bedside procedure has the potential to be both diagnostic and therapeutic for the patient; the importance of this cannot be underestimated).
Multiple authors have demonstrated that anxiety, depression, and stress clearly produce major neurochemical and neuroendocrine changes in the brain (10,11). Changes in neurobiology would be expected to contribute to impaired erectile function. Stress and anxiety lead to increased epinephrine production, and heightened sympathetic tone leads to exaggerated cavernosal smooth muscle contraction, inability of smooth muscle to relax, and subsequent erectile dysfunction (6,7). Failure to achieve a fully rigid erection may aggravate performance anxiety leading to a vicious cycle.
Though psychological causes of erectile dysfunction may be more complex than medical causes, they are still treatable. You should know, however, that resolving psychological impotence may not be quite as simple as taking Viagra (sildenafil citrate). ED drugs are designed to sidestep the physiological causes for ED such as low blood pressure or vascular damage – they won’t help you with issues of anxiety, stress, or low self-esteem. The best treatment for psychological ED will address the problem at its root.
If the patient reports a history of trauma to the genitals that preceded his erectile dysfunction, further evaluation with pharmacologic injection and penile color duplex ultrasound (PCDU) would be indicated to assess for arterial insufficiency or venous occlusive dysfunction (19). Prior to PCDU, however, you might give him a trial of oral PDE5 inhibitors. If those medications are effective, you have effectively ruled out significant arterial insufficiency or venous leakage disease as an etiology. Regardless of outcome of PCDU, no surgical intervention would likely be offered to this man who responds well to oral agents.
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.
Although few studies specifically evaluated the clinical characteristics of ED in younger men, this problem is increasingly frequent. Healthcare professionals both inside and outside of Sexual Medicine are likely to deal with young men complaining for ED and it is important that basic knowledge on this topic is available. In fact, young men reporting ED risk being dismissed without any specific medical assessment, including medical history or physical exam, owing to the assumption that ED in younger is a self-limiting condition, without any clinical consequence. However, evidence shows that, similar to middle-aged or older men, ED can be the consequence of the combination of organic, psychological and relational factors and all these components must be assessed for a correct clinical management. In particular, ED in younger, even more than in older men, can be considered a harbinger of CVD and it offers the unique opportunity to unearth the presence of CV risk factors, thus allowing effective and high quality preventive interventions.
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.
The causes of ED are numerous but generally fall into two categories: organic or psychogenic. The organic causes can be subdivied into five categories: vascular, traumatic/postsurgical, neurological, endocrine-induced, and drug-induced. Examples of the psychogenic causes are depression, performance anxiety, and relationship problems. In people with diabetes, the main risk factors are neuropathy, vascular insufficiency, poor glycemic control, hypertension, low testosterone levels, and possibly a history of smoking.
Sildenafil should be taken 1–2 h before intercourse. It is important to tell patients that the drug’s effectiveness requires sexual stimulation. One patient in our clinic recently complained that he had no effect from taking sildenafil. It was later discovered that he took the pill and then sat on his couch and read a book about how to grow tomatoes!
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).
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For obvious reasons, ED can be a sensitive subject, one that until relatively recently men were more likely to try to hide than to deal with. Fortunately, a deeper understanding of the variety of causes of erectile dysfunction has led to medications, therapies, and other treatments that can be more individualized and more likely to be effective—and more open discussion about addressing the concern.
When a man becomes sexually excited, muscles in their penis relax. This relaxation allows for increased blood flow through the penile arteries. This blood fills two chambers inside the penis called the corpora cavernosa. As the chambers fill with blood, the penis grows rigid. Erection ends when the muscles contract and the accumulated blood can flow out through the penile veins.
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.
There are two kinds of surgery for ED: one involves implantation of a penile prosthesis; the other attempts vascular reconstruction. Expert opinion about surgical implants has changed during recent years; today, surgery is no longer so widely recommended. There are many less-invasive and less-expensive options, and surgery should be considered only as a last resort.
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