Introduction

Vacuum therapy (VT) uses negative pressure to distend the corporal sinusoids and to increase blood inflow to the penis. If a constricting ring is used, VT would be categorized as a vacuum constriction device (VCD); in this setting, an external constricting ring is placed at the base of the penis to prevent blood outflow from the corpora cavernosa, and an erection is maintained for sexual intercourse. A vacuum erectile device (VED) is the use of VT without a constrictive ring, with the objective of increasing blood oxygenation in the corpora cavernosa, among other reasons. As a non-invasive, effective, safe, drug-free and cost-effective erectile dysfunction (ED) treatment, VCD was gradually accepted by the urological community and was finally recommended as an alternative for treatment of ED by the American Urological Association in 1996.1 With the great success of phosphodiesterase-5 inhibitors (PDE5I) for treatment of ED, VCD lost its luster. However, when PDE5I limitations were shown and VED use expanded, interest about VT has been rekindled. This review addresses the applications of VT for ED, penile rehabilitation (PR) and other urological conditions.

History

In 1874, John King, an American physician, stated that ‘when there is impotency with a diminution of the size of the male organ, the glass exhauster should be applied to the part’. What he referred to was simply a vacuum device capable of producing an artificial erection. However, it failed to maintain the erection once the glass exhauster was taken off the penis.2 It was not until 1917, when a patent was granted to Otto Lederer for his ‘surgical device to produce erection with vacuum’, that the concept of a ‘compression’ ring to be used in conjunction with the vacuum device was introduced.3 Since then, several patents had been granted to modifications,4, 5 but the credit for the popularization of VCD is generally given to a Georgian entrepreneur, Geddins D Osbon, who developed his ‘youth equivalent device’ in the 1960s. It was reported that he personally used the device for more than 20 years without device failure while popularizing and perfecting the device. His effort culminated in the first marketed VCD device, Erecaid,6 to receive the US Food and Drug Administration (FDA) approval in 1982.7 Despite this, the device faced strong skepticism among the medical community and patients. Instrumental in overcoming these skepticisms and popularizing the device were the early works of Nadig8 and Witherington9 in establishing its efficacy and safety profiles. It was thought to have finally gained acceptance by the medical community with Lue's commentary in the Journal of Urology: ‘I recommend a vacuum constriction device to all of my patients (except those with coagulation disorders and sickle cell disease) as the initial medical option’.10 As more evidence emerged, the American Urological Association ultimately recommended VCD as one of three treatment alternatives for organic ED.1

Devices and mechanisms

Currently, there are over dozens of commercially available VCDs, that is, Timm Medical Technologies (Eden Prairie, MN, USA), Mission Pharmacal (San Antonio, TX, USA), Encore (Louisville, KY, USA), Mentor (Santa Barbara, CA, USA) and Post-T-Vac (Dodge City, KS, USA). All of these devices share the same basic mechanics since its original development. They all comprise three components: a vacuum cylinder, a battery or manually operated vacuum pump and constriction rings of varying sizes (Figure 1).11 Some of the latest models have a pressure release valve designed to prevent penile injury from excessive negative pressure.12 It is reported that single-handed devices are more desirable to novice users.13

Figure 1
figure 1

Three types of human vacuum devices.

Full size image

Usage begins with placing the correct constriction ring over the open end of the vacuum cylinder. A copious amount of a water-soluble lubricant is then applied to the base of the penis to create a tight seal once the vacuum cylinder is placed over. Negative pressure (100–225 mm Hg) generated either by hand or a battery-operated pump is then applied to create an artificial erection.14 Once the desired state of erection is achieved, the constriction ring is displaced onto the base of the penis to maintain the erect state. Variable vacuum cylinders and constriction rings are available to select for those that are most comfortable and effective. The vacuum cylinders could then be removed and the patient may have intimacy. Patients can become proficient with the device within 5 days15 or four practice sessions.9 The time required to achieve an adequate penile erection ranges from 30 s to 7 min,9, 16 and many manufacturers advise patients to pump for 1–2 min, release and then pump again for 3–4 min.7

Unlike the normal physiology of penile erection in which a complex interplay between neural inputs, vascular patency and hormonal secretion is required, tumescence from VCD resulted from passive flow of mixed venous and arterial blood.17, 18 Broderick et al.17 showed by color Doppler ultrasound that the negative pressure transiently drew arterial blood into the sinusoidal spaces of the cavernosal tissues, increasing its diameter nearly two-fold. The change in diameter owed itself to both intracorporal and extracorporal distention. The constriction ring placed at the base of the penis prevented the venous outflow. Color Doppler ultrasound performed after the placement of constriction ring, however, showed no arterial inflow into the penis.17 Blood gas analysis showed ischemia after 30 min of applying constriction ring.18 This led to the recommendation that the constriction ring should not be left on for >30 min to prevent ischemic injury to the penis. Compared with naturally occurring erections, VCD-derived erections are perceived differently by both the man and their partner. The ‘erection’ looks dusky and feels cooler than normal, with increased volume distally, especially at the glans penis.7

VT in erectile dysfunction–VCD

Indications

VCD therapy can be applied successfully for nearly all etiologies of ED;8 although its success depends on appropriate instruction and practice.19 More than 90% of men will experience functional erection with VCD therapy with adequate practice.9

It is currently a second-line therapy along with intracavernosal self-injection and intraurethral therapy with vasoactive substances.20 It is widely believed that VCD therapy is more acceptable among elderly patients with occasional sexual intimacy, as younger patients may show limited acceptance because of its perceived ‘unnatural’ erection.21 Chen et al., conversely, reported that VCD therapy remained the preferred treatment option among couples who had achieved satisfactory erections with either VCDs and PDE5I.22

VCD may also be used in conjunction with other therapies for synergistic effects. It has been reported that VCD therapy could be combined with PDE5I,23 intracavernosal self-injection,24, 25 intraurethral therapy,26 psychotherapy27 and even penile prosthesis.28, 29

Contraindications

Contraindications to the use of VCD are few and primarily include patients with a tendency for spontaneous priapism or intermittent prolonged erections, and those with severe penile anomalies (either congenital or acquired).7 There are some relative contraindications, which can be overcome by education and precautious care, such as cultural taboo, cervical or high-thoracic spinal cord injuries, neurological disease or degenerative joint diseases with poor manual dexterity.30 Patients with bleeding disorders or those on anticoagulation therapy are considered at high risk to develop petechiae, eechymosis or hematoma;7 however, it was shown that the risk did not exceed that of the general population.31

Clinical results

VCDs, unlike PDE5Is, have not had to undergo strict clinical trials to show their safety and efficacy before their widespread usage. A review of literature consists largely of single-center observational series, collection of small prospective clinical trials and commercial databases. Despite the paucity of data, a wealth of clinical experience is available, although with big variability in the clinical efficacy of VCD therapy. These data are present in Table 1.

Table 1 Efficacy of VCDs
Full size table

Nadig et al. were the first to provide objective data regarding penile rigidity obtained using VCDs. It was found that buckle pressures of 454 g (the minimal criterion for rigidity used by many sleep laboratories) were achieved in 27/35 (77%) patients.8 Bosshardt and co-workers showed that a nocturnal penile tumescence rigidity of 80% (70% being sufficient for intercourse)40 was the norm after 6 months in their group of 26 patients. They also showed that induced ischemia could result after 30 min of applying the constriction rings. This led to the recommendation that the constriction ring should not be left on for >30 min to prevent ischemic injury to the penis.18

The effectiveness of VED has been established for different causes of ED. For those with arteriogenic ED, VCD therapy achieved the efficacy and satisfaction rates of 67 and 84%, respectively.37 For the corporeal veno-occlusive dysfunction ED, Kolettis et al.38 reported a 56% satisfaction rate. For diabetic ED, Arauz-Pacheco et al.41 and Bodansky et al.42 reported successful rates of 75 and 58%, respectively. No severe side effects were reported. For spinal cord injury-induced ED, an impressive 85% successful rate was achieved with minor side effects.43 The largest patient group (34 777 cases) was reported by Lewis and Witherington7 who used the VCD data from Osbon data bank with satisfaction rates 65–83%; however, only 17% (5847) cases had enough information to evaluate. Conversely, Vrijhof et al.36 and Sidi et al.16 reported much lower satisfaction rates, 50 and 68%, respectively. More dramatically, Dutta et al. reported only 35% satisfaction rate, with an attrition rate of 65%.39 It is believed that the huge discrepancy of satisfaction rates may be attributed to patient selection and patient education.

Complications

The use of VCD is usually well tolerated with mostly mild side effects (Table 2). The most common side effects include numbness, pain, penile bruising or petechiae.9, 32, 37, 44, 45, 46 Due to the constriction rings, painful ejaculation or sensation of trapped ejaculate has also been commonly reported.7, 9 Other rare complications such as leg spasms, testicular migration, urethral varicosities/bleeding have been reported.47 Major complications like Peyronie's disease, penile skin necrosis, penile gangrene and Fournier's syndrome have been reported anecdotally.47, 48, 49, 50, 51, 52

Table 2 Complications of VCDs
Full size table

VT in penile rehabilitation—VED

Introduction

Prostate cancer is the most common solid-organ cancer among men and one of the leading causes of death.53 With early detection and radical prostatectomy (RP), the 15-year overall actuarial cancer-specific survival rate has reached 90%.54, 55 Unfortunately, RP is associated with several quality-of-life side effects, mainly urinary incontinence and ED.56, 57 With improvements in technique and the use of robotic-assisted procedures, incontinence rates have reduced to an acceptable level.58, 59, 60, 61 However, the same cannot be said for ED, as the incidence of ED after RP ranges from 10 to 100%.62 In an attempt to improve patients’ quality of life after RP, PR is now widely applied in clinical practice.55, 63, 64, 65 Currently, PR methods include the use of PDE5I, intracavernosal self-injection/intraurethral suppositories, VED or a combination of different therapy modalities.55, 63, 64, 65

Pathophysiology

Erectile function (EF) becomes impaired immediately after RP secondary to cavernous nerve damage during surgery, resulting in neuropraxia.66 Even with the most meticulous nerve-sparing dissection, some degree of neuropraxia is unavoidable because of the close proximity of the nerves to the prostatic gland. These nerves tend to recover slowly, and it may take as long as 3 years for them to return to a new baseline functional status.58 Absence or decreased erection and penile size ensue before recovery of the cavernous nerve.57, 67 A reduction in arterial inflow has also been reported due to ligation of the accessory internal pudendal arteries during RP.68, 69 The combination of nerve damage with decreased arterial inflow may cause penile tissue hypoxia leading to apoptosis and collagen deposition, which ultimately results in venous leak, which in turn, has been linked to the pathophysiology of ED after RP.70, 71, 72, 73, 74, 75, 76, 77, 78, 79 As nerve recovery requires time, it is hypothesized that VED may bypass the neuropraxic period by directly dilating the cavernosal arteries, therefore, overcoming hypoxia and preventing apoptosis and fibrosis before the functional recovery of the cavernous nerve.

Laboratory and clinical evidence

VED, as PR modality, simulates natural erection and allows reoxygenation of the penis.80 There has been growing evidence to support this. Blair et al.81 documented that sub-atmospheric pressure induces an initial increase in arterial inflow in the forearm of healthy volunteers; Greenfield and Paterson82 further showed a vasodilation effect on the arteries of the forearm in volunteers exposed to a sub-atmospheric pressure of −150 to −200 mm Hg, which is similar to the pressure used in VED.14 Diederichs et al.83 noticed that negative pressure induces expansion of penile tissue followed by increase in blood flow in primates; the authors believed that the increased blood flow was arterial inflow. Broderick et al.17 showed that a transient vacuum application increases the peak flow velocity of the cavernous arteries in humans. Donatucci and Lue84 further determined that chronic VED usage increases cavernous arterial flow in men with mild vasculogenic ED as measured using a duplex ultrasonograph. Bosshardt et al. performed blood gas analysis before VED application, immediately after the application of a constriction ring and repeated blood gas analysis 15 and 30 min later with the constriction ring in place in ED patients. This test showed that the mean O2 saturation of corporal blood immediately after VED-induced erection was 79.2%, which translates as arterial and venous contributions of flow of 58 and 42%, respectively. In addition, after 30 min of continuous application of a constriction ring, blood gas analysis showed ischemia of the penile blood.18 This is the rationale for the use of VED as PR modality, instead of VCD. Recently, Müller et al.85 applied hyperbaric oxygen therapy on a bilateral cavernous nerve crash rat model and showed that hyperbaric oxygen therapy improved the preservation of EF. To explore the molecular mechanism of VED, a rat-specific VED, which simulates human VED, was successfully created and applied on a bilateral cavernous nerve crash model by our group.86 Our preliminary data indicated that daily VED therapy significantly improved the intracavernosal pressure/mean artery pressure ratio, preserved penile length and girth, decreased the level of hypoxia-inducible factor-1α, transforming growth factor-β1, collagen and apoptosis, and increased the level of eNOS and α-smooth-muscle actin.87

The latest PR trials are summarized in Table 3.88 Most trials used PDE5I to preserve penile sexual health. One limitation of PDE5I is its requirement of intact nerves to produce nitric oxide for proper function. There have been theories that PDE5I may work through a separate, neuron-independent endothelial cell mechanism; however, it is still unproven.80 The direct mechanism of VED circumvented this limitation. Given its low complication rate and relatively high compliance rate, along with being the only modality that preserves penile length, VED is an ideal choice as PR after RP80 or other pelvic injuries.97, 98

Table 3 Summary table of penile rehabilitation trials
Full size table

Munding et al.99 documented that up to 48% men had considerable shortening of the stretched penile length (greater than 1.0 cm) at 3 months after RP. Savoie et al.100 found that nearly 20% of men who undergo RP experience a penile length loss greater than 15%. Gontero et al.101 followed 126 men who had undergone RP and measured penile length before surgery, at the time of catheter removal, and then at 3, 6 and 12 months. They found that the greatest amount of shrinkage occurs in the immediate postoperative period, although shortening continues at a lesser rate throughout the entire study period. They also found that a return of EF, defined as an International Index of Erectile Function (IIEF) of 15, and a nerve-sparing technique during RP, mitigated penile shaft shrinkage. Several studies looking at the efficacy of VED in preserving EF have also examined preserved penile length as a secondary endpoint.

Raina et al.92 randomized 109 post-NSRP patients to early VED daily usage (group-1, n=70) versus no erectogenic aid (group-2, n=35). The participants were followed by the Sexual Health Inventory for Men (SHIM) score. The secondary endpoints included compliance, changes in penile circumference or length, return of natural EF and ability for vaginal intercourse. At the end of the 9-month follow-up, 80% (60/74) of those in group-1 were able to have sexual intercourse using the device, with a satisfaction rate of 55%. Nineteen patients reported return of natural erections and 17 had erections sufficiently firm for vaginal penetration. Conversely, only 37% (13/37) of the patients in group-2 regained natural erections. When evaluating for secondary endpoints, among those who used the device regularly, only 23% (14/60) reported a decrease in penile length and girth, whereas 22/35 (60%) patients in the control group complained of penile shrinkage. This result was confirmed by Dalkin et al. who administered VED therapy to 39 men after RP for 90 days after catheter removal.102 In their study, 97% of compliant men maintained their preoperative stretched penile length; shrinkage was defined as ⩾1 cm. The authors concluded that early usage of VED facilitates early return of spontaneous EF, early resumption of sexual life resulting in spousal satisfaction and preservation of penile length and size.

Other authors have investigated the timing of VED therapy to maximize its benefits. Köhler et al.93 randomized 28 patients undergoing RP to early VED use (group-1, n=17) and delayed VED use (group-2, n=11). Group-1 was instructed to use VED daily, starting at 1 month after RP for two consecutive 5-min periods. Group-2 was instructed to use VED, as many times as desired, starting at 6 months after RP. These men were followed using IIEF scores. At a follow-up of 3 and 6 months, group-1 had a statistically higher IIEF score than group-2. Beyond 6 months, when group-2 began using VED therapy, there was no statistical difference in IIEF scores between both groups. When evaluating for penile shortening after RP, group-1 did not experience any significant penile length reduction; whereas group-2 experienced considerable shrinkage at 3 months (mean loss 1.87 cm) and 6 months of follow-up (mean loss 1.82 cm). However, when group-2 began using VED therapy, the mean penile length loss decreased to 1 cm. The authors concluded that early VED therapy after RP helps to improve early sexual function and preserve penile length.

Solid evidence that VED daily rehabilitation preserves penile length and EF has been scattered; however, a multicenter, randomized study with objective criteria and long-term follow-up is still needed.

VT under other urological conditions

In addition to its applications for ED and PR, VT has been expanded to other urological conditions. VED has been regarded as an initiator and enhancement of other ED therapies. Bellorofonte et al.103 showed a synergistic action between intracavernosal vasoactive agents and VT. John et al.26 combined VED with intra-urethral prostaglandin E1 to eliminate the need for constriction ring, with 100% successful rate in 19 patients. Cecchi et al.104 evaluated VT with topical minoxidil in 18 patients and found that the combination enhanced the erection quality, reduced the time of device application and avoided 67% (12/18) the need for constrictive rings.

VED has also been used to preserve or restore natural potency. Oakley et al.11 speculated that VED usage may delay the onset of intractable impotence in high-risk groups, such as those with diabetes and dyslipidemia. Colombo et al.105 showed that daily VED with or without weekly intracavernosal papaverine (20 mg) injection for 6 months showed significant improvement in spontaneous erectile ability (VED only: 54% (14/26 patients); VED+papaverine: 65% (17/26 patients)). In addition, VED therapy has been shown to have penile length preservation effect in both non-NSRP and NSRP.92 VED has also been successfully used in patients after penile prosthesis removal. Moul and Mcleod106 reported 91% (10/11 patients) satisfactory erection and successful intercourse with the same or better length and circumference, compared with the previous natural erection. The authors attributed the prevention of penile scarring and shortening to the gradual resolution of corporeal scarring, with progressively improved blood flow into corporeal sinuses by the VED therapy. Lue and El-Sakka107 have reported that chronic intermittent stretching with VED successfully lengthened the shortened penis due to severe Peyronie's disease after venous grafting in three patients. Lastly, anecdotal evidence from Oakley et al.11 indicated that VED alone improved the size of both the flaccid and the erect state of the microphallus. However, a program of penile stretching with VED showed no statistically significant difference after 6 months of therapy; although it showed a 30% rate of patient satisfaction, probably due to psychological effect.108

Some VED derivatives have been invented. Gus’kov109 in 2003 reported a combination of the vacuum effect along with vibration—the vibrovacuum fallostimulator named ‘Sanos’. The author claimed that this new device reduced the exposure of the penis to the vacuum effect, thus preventing edema, hemorrhage and necrosis of the penile skin. He also claimed that this had an efficacy rate of 92.1% among 330 patients; however, no further confirmatory report has been found. Another version of VED is the EROS-CTD (Clitoral Therapy Device; UroMetrics Inc., St Paul, MN, USA), the only FDA approved mechanical treatment for female sexual dysfunction. This device causes clitoral vascular engorgement using a vacuum system.110 Billups et al.111 reported that a 3-month Eros therapy improved sensation (90%), vaginal lubrication (80%), orgasm (55%), and sexual satisfaction (80%) without adverse effects in 20 women with female sexual dysfunction. Wilson et al.112 confirmed the results in 10 women with female sexual dysfunction. Schroder et al.113 found that the Eros therapy significantly improved patients’ arousal, lubrication, orgasm and desire among 11 women with cervical cancer treated with radiation therapy and sexual arousal and/or orgasmic disorder. Billups et al. showed similar results in terms of vaginal lubrication (92%) and orgasm (62%) for 13 women with female sexual dysfunction and diabetes.114 Many women in this study also noted that after using the Eros therapy several times per week over a 2- to 3-month period, they continued to have improved vaginal lubrication, genital sensation or orgasms even without the device.

Future prospects

VCD therapy is an established alternative for ED therapy when PDE5I therapy failed, contraindicated or became unaffordable. As a variation of VCD, VED has been expanding to more urological conditions that are difficult to manage. The most striking use of VED is penile rehabilitation after RP or other pelvic injuries. As data are increasingly being accumulated from clinical and basic research, the movement is gaining support to establish VED therapy as the centerpiece of PR protocol for post-prostatectomy/pelvic injuries. VT in general will be an indispensable modality in the urological armamentarium for the management of ED and related conditions.