Erectile dysfunction after fracture of the pelvis

Male sexual dysfunction after fracture of the pelvis is more common than previously supposed with rates as high as 30% reported when the complaint is specifically sought. With the increase in survival from major injuries, the long-term consequences of trauma are being seen with increasing frequency. This review addresses the current understanding of the incidence, mechanism of injury, pathophysiology, acute management, subsequent investigation and long-term treatment of erectile dysfunction after injury to the pelvis.

The intimate relationship of the soft tissues and the bony pelvic ring result in a high risk of concomitant local injury associated with fractures of the pelvis.1 The bladder and urethra are particularly vulnerable, with reported rates of injury of 5% to 10%.1-4 Even without severe urological injury, damage to the delicate vascular and nervous tissues supplying the genitalia can result in sexual dysfunction.5,6 Patients with polytrauma often have prolonged stays in hospital and require multiple operations on the pelvis, putting genitourinary structures at further risk of injury.

Erectile dysfunction has been defined as the inability to achieve or maintain an erection adequate for sexual satisfaction. In 3% of patients with sexual dysfunction, this will be secondary to an episode of pelvic or perineal trauma.8 In younger impotent patients, often at the beginning of their sexual lives, the motivation to restore function is very high.

Incidence of erectile dysfunction after pelvic trauma

Few studies have reported the overall incidence of sexual dysfunction after fractures of the pelvis, most concentrating on patients with urethral injury. King,9 in a review of 90 patients published in 1975, found an incidence of 5% of dysfunction in patients without urethral injury, rising to 42% when urethral injury had occurred. Machtens et al,10 in 2001 described an overall incidence of 11.6% in men in a series of 1722 patients who had suffered fractures of the pelvis. Although this is the largest number reviewed to date, the methods used for assessment were not stated. Malavaud et al11 used a previously validated scale to assess erectile dysfunction in 46 patients who had recovered from pelvic fractures. Their patients reported significantly lower scores in sexual satisfaction than normal historical controls, although the latter group was of a higher mean age by 20 years. Eleven patients had significant impairment of sexual function. The only characteristic of the fracture which correlated positively with impaired sexual potency was diastasis of the symphysis pubis. A trend towards impairment after urethral injury was also observed, although this did not reach statistical significance. The rates of incidence which have been reported are summarised in Table I. This suggests that, taking the data as a whole, impotence is seen in about 42% of patients who have a urethral injury. The overall rate of dysfunction after fracture is likely to be higher than the historical figure of 5%,9 lying somewhere between 11%10 and 30%11 depending upon how dysfunction is assessed.

Pathogenesis of erectile dysfunction after pelvic trauma

A strong association between urethral disruption and subsequent impotence is well documented. The prostatic urethra is particularly vulnerable to shearing forces, being fixed by the urogenital diaphragm and puboprostatic ligaments to the ischiopubic rami and the symphysis pubis.1,3,12 Upward or posterior displacement of the symphysis will therefore subject the fixed urethra to considerable stress. Direct laceration by bone fragments is rare.

Erectile dysfunction after injury to the pelvis is due to a combination of neurogenic, vascular, corporal and psychogenic injury.9,13-16 Table II summarises the information available in the literature on the pathogenesis of impotence in these patients.

Neurogenic injury. Severe neurological injury, particularly involving the lumbosacral plexus, may occur at the time of the initial injury and during subsequent operations. The quoted incidence varies widely from less than 1% to more than 30%.16-20 Majeed18 found clinical evidence of neurological injury, confirmed by EMG studies, in 33% of patients with unstable fractures of the pelvis, but only 16% were identified on admission. All patients showed at least partial recovery by three to 12 months, continuing for up to 24 months. Of these, 13 patients were impotent; six recovered. The efferent nerve fibres supplying the cavernous bodies lie within the cavernous nerves to the urethra and symphysis pubis can be injured in isolation without other obvious neurological impairment as they leave the bony pelvis. Unfortunately, there is no specific test for neurogenic erectile dysfunction. The diagnosis is suggested by an abnormality in testing for nocturnal tumescence in association with normal haemodynamic studies.8

Vascular injury. Major vascular damage has been described in patients with impotence after pelvic fracture. The vessels may be lacerated directly or by damage to the intima leading to thrombosis.21 Sharlip22 described obliteration of both the internal pudendal arteries at the level of the urogenital diaphragm on arteriography in three patients. They remained impotent despite formation of collateral vessels and retrograde filling of the dorsal and deep penile arteries. A traumatic arteriovenous fistula between the internal iliac vessels has been described as causing impotence.23 The symptoms resolved after surgical correction.23

Levine et al14 investigated impotent patients, who had suffered blunt perineal or pelvic trauma, using selective internal pudendal arteriography. All of those with a fracture had suffered injury to the posterior urethra. Vascular lesions were identified in both hypogastric-cavernous beds in all patients. Lesions of the pudendal or common penile arteries were seen in 90% of those with a fracture as opposed to 35% of those without. However, 48% of the latter group were more likely to have had an isolated lesion in the cavernous artery compared with only 8% in the group with a fracture. Similar lesions were observed in a control group with vasculogenic impotence but with no history of trauma, although proximal lesions were more common.

Munarriz et al24 investigated a similar group of patients, 42 of whom had suffered fractures of the pelvis. All those with fractures, and 96% overall, had an abnormality of the cavernosal response to pharmacological stimulation, suggesting that there was a haemodynamic component to their pathology; 80% of patients who had sustained trauma to the pelvis had an abnormality of venous outflow and 70% an abnormality of venous occlusion. All the patients with fractures who underwent cavernosography had abnormal findings, 97% of these being proximal, site-specific leaks into local venous structures. Leaks were seen at three or more sites in 60%, the most common being the crural and cavernous veins and the proximal corpus spongiosum. This venous abnormality was more common than in the patients who had not suffered a fracture. Angiography again detected widespread lesions, most frequently in the common penile and cavernous arteries. They concluded that the most likely cause of the widespread venous leak was the direct impact of the fixed proximal corpora against the pubic rami or a shearing effect at the point of fixation. Purely arterial damage was noted in 30% of the patients indicating that they might respond to microsurgical revascularisation.8 Veno-occlusive abnormalities in patients with erectile dysfunction in general are unlikely to be related to a venous anomaly but probably represent inadequate function of smooth muscle which may be secondary to arterial disease or neural damage.25 This may also be the case in those with a fracture.

Corporal injury. While the penis itself is free and therefore relatively protected from the effect of blunt trauma, the corpora are attached to the undersurface of the ischiopubic rami. This makes them vulnerable to shearing forces during fracture. Such injury could induce fibrosis during healing, subsequently impairing the ability to dilate.8 MRI has shown a high incidence of injury to the corpora in patients with a fracture, urethral injury and impotence. Armenakas et al26 demonstrated injuries in 12 of 15 patients examined, including eight avulsions and four fractures. Doppler imaging revealed that 12 patients had primarily vasculogenic impotence with low peak flow velocities, and three had neurogenic impotence. Of the vasculogenic group, five had a significant venous leak as shown by large rates of diastolic flow. These were associated with severe injury to the corpora in four patients and it may be that fibrosis may also interfere with the complex veno-occlusive mechanisms.26 Such injuries may lead to the formation of venous fistulae, allowing abnormal leakage of blood.