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Sexual Dysfunction Following Abdominal Aortic Aneurysm
Introduction
Following the successful management of the initial life-threatening sequelae associated with the surgical repair of ruptured abdominal aortic aneurysm (AAA), the quality of the life saved requires continued consideration. Postoperative sexual dysfunction represents a significant, underdiagnosed consequence of this condition, yet many treatment options exist.
Case History
A 72-year-old man attended a routine outpatient appointment one year after undergoing emergency surgical repair of a ruptured infrarenal AAA. He had presented at that time with back pain and systemic hypotension (90/40 mmHg). The diagnosis was confirmed by computerised tomography (which demonstrated a 6 cm infrarenal AAA with evidence of retroperitoneal extravasation). He was taken immediately to the operating room where he underwent a seemingly uncomplicated laparotomy and aneurysm repair (aortic cross-clamp time = 75 minutes, mean arterial pressure intraoperatively = 60 mmHg). Although he subsequently appeared to make an uneventful recovery, at the time of follow-up he indicated that he was suffering from sexual impotence (he euphemistically stated, “I am unable to have any more children.”). Further questioning established that he had erectile dysfunction only since the time of surgery, although he maintained normal nocturnal penile tumescence. Co-existent risk factors for impaired sexual performance included his age and prior smoking history (35 pack-years), along with the presence of hypertension (treated with propanolol), hypercholesterolaemia, peripheral vascular disease and ischemic heart disease. He did not, however, have diabetes mellitus. After consultation with, and review by, the urological service in the hospital, he was commenced on sildenafil (Viagra, Pfizer, New York, New York), and reported significant improvement soon after commencing this therapy.
Discussion
Although it has long been clear that aorto-iliac occlusive disease is often associated with male sexual dysfunction, it has only recently been realized that operative repair of AAA disease can impair potency.1 Furthermore, while female sexual function has been considered immune to the iatrogenic effects of vascular reconstructive surgery, studies utilizing more sensitive sexological tests suggest a degree of impairment may arise due to perioperative events in women as well as men.2 However, although the rate of sexual dysfunction after AAA approximates 50% (and may be as high as 80%), accurate recognition of this devastating problem is often confounded by co-existing precipitants of compromised sexual dysfunction (including smoking, antihypertensive medications, diabetic-associated arteriopathy and neuropathy, atherosclerotic compromise of internal iliac circulation and psychological reaction to major surgery for life-threatening disease).3,4
Additionally, the effects of major operative intervention on the psyche (including situational depression and alteration in perception of body image), may exacerbate any physical diminution in sexual capacity.
Male potency depends on a neurogenically-instigated vasodilation of the penile corpora cavernosum. Although parasympathetic innervation (arising from the second to fourth lumbar segments) primarily initiates the erectile response to sexual stimulation, and the sympathetic chain (11th thoracic to 2nd lumbar segments) induces ejaculation, considerable intercommunication and overlap exisits between both pathways at the level of the paraaortic and superior hypogastric plexuses. Operatively, dissection along the anterior surface of the aorta and, in particular, over the left iliac artery, can injure the neural bundles running from the spinal cord and can result in diminished or eliminated innervation. Diminished nerve stimulation can compound what can already be an impaired vascular response (due to arteriopathy of the hypogastric artery and its distal branches), and thus result in impotence. In addition to trauma-related autonomic neuropraxia, the act of cross-clamping the aorta during open repair results in pelvic and penile ischemia, an effect exacerbated by pre- and intra-operative hypotension (a situation more likely in cases of emergent repair). Additionally, periaortic hematoma-associated retroperitoneal aneurysm rupture can also compress nerve trunks and branches. Finally, on completion of the graft inlay, venting thromboembolic debris down the internal iliac artery is often performed, as it is deemed preferable to risking peripheral limb artery embolic occlusion. The internal location of the female sex organs is believed to confer a protective effect against peroperative injury, as it allows them a more highly collateralized blood supply than in the male. Furthermore, female sexual sensation tends to be more dependent on the integrity of the endofascially-protected pudendal nerves than on the peri-aortic nerve plexuses.
Although careful surgical technique can minimize the occurrence of significant, iatrogenic injury, it has been proposed that endovascular approaches may obviate the risk of operative neurogenic injury altogether, and aortic stenting may become the procedure of choice for sexually active patients on this basis.5 However, this assumption has been somewhat undermined by the Dutch Randomized Endovascular Aneurysm Management (DREAM) trial, which despite showing a quicker return to normal sexual function in the endovascular group, demonstrated no significant difference after one year follow-up.6,7 The pharmacological armamentarium of postoperative impotence treatments has been significantly bolstered by the arrival of sildenafil. The augmentation of the vasodilatory response to neural stimulation means that it is of potential benefit to the majority of sufferers, even those with predominantly neurogenic impotence.8 While the caution required in prescribing this drug for those taking nitrate therapy for cardiovascular disease may limit its usefulness in many patients with peripheral vascular disease, it nonetheless represents a significantly more patient-friendly alternative to the previous mainstays of impotence therapies, including vacuum-assisted mechanical devices and cavernosal injection therapies.
In summary, improved awareness of this condition can facilitate more comprehensive preoperative consenting of patients and minimize the risk of traumatic injury to vital structures during surgery. It also allows early postoperative identification, reassurance and treatment. Reticence on the part of patients to report, and of physicians to inquire, about sexual performance, acts to only minimize the frequency with which the problem is identified.
1. Leriche R. Des obliterations arterielles hautes (obliteration de la terminaison de l’aorte) comme causes des insufficances circulatoires des membres inferieurs. Bull Mem Soc Chir 1923;49:1404.
2. Hultgren R, Sjogren B, Soderberg M, et al. Sexual function in women suffering from aortoiliac occlusive disease. Eur J Endovascular Surg 1999;17:306–312.
3. Magee R. Sexual function after aortic surgery. ANZ J Surg 2003;73:572–576.
4. Lee ES Kor DJ, Kuskowski MA, Santilli SM. Incidence of erectile dysfunction after open abdominal aortic aneurysm repair. Ann Vasc Surg 2000;14:13–19.
5. Dougherty MJ, Calligaro KD. How to avoid and manage nerve injuries associated with aortic surgery: Ischaemic neuropathy, traction injury and sexual derangements. Semin Vasc Surg 2001;14:275–281.
6. Xenos ES, Stevens SL, Freeman MB, et al. Erectile function after open or endovascular repair. Ann Vasc Surg 2003;17:530–538.
7. Prinssen M, Buskens E, Nolthenius RP, et al. Sexual dysfunction after conventional and endovascular AAA repair: Results of the DREAM trial. J Endovasc Ther 2004;11:613–620.
8. Blander DS, Sanchez-Ortiz RF, Wein AJ, Broderick GA. Efficacy of sildenafil in erectile dysfunction after radical prostatectomy. Int J Impot Res 2000;12:165–168.
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