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Postoperative erectile dysfunction

Vascular surgery in the aortoiliac region

With the progressing development of vascular surgery and the anesthesiologically intensive medical possibilities, an increasing number of reconstructive interventions in the area of the abdominal aorta are performed. Preoperative erectile dysfunction in the context of general angiosclerosis can be surgically corrected only to a very limited extent. Isolated occlusions in the supply area of the internal iliac artery can possibly be surgically corrected at the same time. Postoperative erectile dysfunction, on the other hand, is much rarer after prosthetic aortic replacement than ejaculatory dysfunction. The latter may be primarily due to damage to the sympathetic superior hypogastric plexus by the operation, as is also known to occur after radical retroperitoneal lymphadenectomy for the treatment of nonseminomatous testicular tumors. In young men, this operation rarely leads to impaired erection, but ejaculatory dysfunction must be expected in up to 90% of the cases. For older men with completed family planning, the harmless postoperative retrograde ejaculation should not be significant, but postoperative erectile dysfunction impairs the quality of life. It is not clear why erectile dysfunction occurs more frequently (approx. 17%) in this older patient group than in younger patients. It is assumed that the sympathetic nerve damage leads to increased limb perfusion and thus to a vascular steal phenomenon of the supply to the internal genitalia, which has an additional unfavorable effect, especially in the case of reduced perfusion. High lumbar sympathectomy with bilateral excision of the borderline ganglia TH12, L1, and L2 has also been reported to result in the occurrence of erectile dysfunction [20]. A similar mechanism may be responsible for erectile dysfunction in spinal ice grips (spondylodesis anterior). A. V. Hochstetter [17] has recommended a retromesenteric approach to the aortoiliac area to prevent these neurogenic disorders, which was able to reduce postoperative ejaculatory disorders from 81% to 20%, but postoperative erectile dysfunction only from 17% to 12% in comparative collectives of different sizes. In conclusion, before aortoiliac vascular procedures, patients should be educated about the possible occurrence of ejaculatory dysfunction and about erectile dysfunction, which is much less common.

4.4.2 Rectal extirpation

Postoperative erectile dysfunction must be expected after radical surgery for rectal cancer, and it is much more common after abdominoperineal rectal amputation than after continence-preserving anterior rectal resection. The damage is understood to be nerve-related due to injury to the parasympathetic branches from S2-S4 running in the vascular-nerve bundle in the lateral portions of the prostate, but vascular-arterial involvement of the pudendal arteries is also conceivable. With more extensive damage to parasympathetic structures, neurogenic bladder voiding dysfunction may also be found postoperatively. Special erection-protective surgical techniques have been developed by Stelzner [22] but are not always successfully applicable depending on tumor location and extension. While erectile dysfunction can be expected to be around 25% in malignant diseases, the rate in colorectal surgery of benign diseases (proctocolectomy for ulcerative colitis, Crohn's disease) is only around 2-4%. In tumor surgery, there is a clear age dependence of postoperative erectile dysfunction. An impotence rate of 100% has been reported in patients older than 70 years at the time of surgery. Spontaneous recovery of erectile function is still possible up to about one year after surgery. In general, erectile dysfunction after abdominoperineal surgery has been reported to respond to vasoactive substances (4 patients in our own patient population).

4.4.3 Radical cystoprostatovesiculectomy and radical prostatovesiculectomy

In earlier years, after radical removal of the prostate for 10-calcific prostate carcinoma, erectile dysfunction was expected to be in the order of 60% (85%). After cystoprostatovesiculectomy for bladder carcinoma, the rate of postoperative erectile dysfunction was as high as 100%. Walsh [25] presented a new surgical technique that allows identification and sparing of the vascular-nerve bundle that runs in the lateral portions of the prostatic fascia. In non-capsular infiltrating prostate carcinoma, the rate of postoperative erectile dysfunction was reduced to as low as 15%. After radical cystoprostatovesiculectomy, the rate of postoperative erectile dysfunction was reduced to 67%. Although a combination of arterial and neurogenic factors can be suspected based on the mechanism of injury, diagnostic testing should not be omitted. Positive results of arterial revascularization have been reported when arterial circulatory dysfunction is demonstrated. In general, after radical prostatectomy, there is a response to vasoactive agents (10 patients in our own patient population). SKAT responders and SKAT non-responders have been seen after radical cystoprostatovesiculectomy. Spontaneous recoveries of erectile function seem to be possible even after a very long time, as the following casuistry illustrates:

A 62-year-old patient undergoes radical prostatectomy for locally confined prostate carcinoma in June 1988. SKAT therapy is started 8 months postoperatively with 1 ml of a papaverine-phentolamine mixture (15 mg papaverine/0.5 mg phentolamine) because spontaneous recovery of erectile function is no longer expected. The patient is followed up regularly. After one year, he no longer presents to the andrology consultation. In January 1991, the patient, who has received further care elsewhere, is seen by chance at a tumor follow-up. The follow-up examination reveals no evidence of progression of the underlying condition. Asked about the earlier SKAT therapy, the patient states a complete return of erectile function after one year of SKAT therapy.

4.4.4 Transurethral prostate resection (TURP)

Literature data on the incidence of erectile dysfunction after transurethral prostate resection for prostatic adenoma are contradictory (Table 4.1). It should also be noted that a not inconsiderable proportion of the generally elderly patient population could already have impaired erectile function preoperatively. Jameson [7] reported an incidence of erectile dysfunction of 4% in 1600 patients. Gold [6] reported impotence rates of 10 to 66% depending on age. In the 50- to 60-year-old group, the rate of postoperative erectile dysfunction was 10%; however, 10% of patients also reported improvement in erection postoperatively. In the 70- to 80-year-old group, the rate of postoperative erectile dysfunction was 66%, demonstrating a clear age dependence in the incidence of erectile dysfunction after prostate resection.

Table 4.1. Incidence of erectile dysfunction after TURP (literature review).

Incidence of erectile dysfunction after TURP

The surgical technique (suprapubic adenomectomy or transurethral prostate resection) did not influence the manifestation rate. Libman [13] criticized the methodological weaknesses of all studies conducted to date on the incidence of erectile dysfunction after prostate resection. All studies lack pre- and postoperative determination of objective parameters. However, it can be assumed that excessive electrocoagulation in the 5- and 7-o'clock positions may have a negative effect on cavernous nerves with secondary erectile dysfunction in a proportion of patients [7]. In our own patient population, 8 of 10 patients presenting for erectile dysfunction after transurethral prostatic resection had no or inadequate response to vasoactive agents (Fig. 4.7). Another example of an objective negative influence of prostate resection on erection is given by the following casuistry:

A 75-year-old, biologically much younger patient has been undergoing SKAT therapy with a papaverine-phentolamine mixture (30 mg papaverine / 1 mg phentolamine) for 6 months due to erectile dysfunction. With the dose used, a fully rigid erection of 1 h duration can be provoked. Due to increasing micturition difficulties, a transurethral prostatic resection has to be performed. The patient presents to the andrology consultation 3 months postoperatively, claiming that the injections are now no longer working. Up to 4 ml of a papaverine-phentolamine mixture (60 mg papaverine / 2 mg phentolamine) is injected during self-administered tests, but unsuccessfully. Subsequently, up to 40 mg of prostaglandin is injected, but this also shows no success. It is finally possible to provoke erections sufficient for cohabitation again with a papaverine-phentolamine-prostaglandin E1 mixture. The patient then continues therapy with this mixture.

65-year-old patient with erectile dysfunction after transurethral prostate resection

Fig. 4.7. 65-year-old patient with erectile dysfunction after transurethral prostate resection (resection weight 26 g); SKAT-non-responder; cavernosographic outflow of contrast agent via the periprostatic plexus.

4.5 Radiogenic erectile dysfunction

The occurrence of erectile dysfunction after pelvic irradiation is a potential complication that must be reported, particularly in the case of radiation therapy for prostate carcinoma. Data on the frequency vary between 22-84% [20]. For interstitial radiation, the incidence of postoperative sexual dysfunction is said to be more favorable [5]. According to Goldstein [6], radiotherapy is said to accelerate arteriosclerotic changes in the iliac arteries. Accordingly, the erectile dysfunctions induced by it were mainly of arterial origin. However, the sometimes abrupt onset of symptoms with the start of therapy in some patients also casts doubt on this hypothesis. In radical prostatectomy of previously radiotherapied patients, the vascular-nerve bundle is found in a thick scar plate, so that compression occlusion of the arteries in this area also seems possible.

4.6 Diabetes mellitus

About 50% of patients with diabetes mellitus are expected to develop erectile dysfunction during their disease [18]. Erectile dysfunction may also be the first clinical manifestation of as yet unknown diabetes mellitus. Aetiologically, micro- and macroangiopathy of the penile vessels, neuropathy, but also damage in the cavernous tissue [13] must be included in the differential diagnostic considerations. In vitro studies of isolated corpus cavernosum strips from impotent diabetic patients also demonstrated that endothelium-dependent relaxation of the tissue was attenuated [24]. During the diagnostic workup, SKAT responders and SKAT non-responders are found. The workup should definitely include a bladder function examination, since bladder voiding dysfunction may be the first sign of autonomic neuropathy. Therapeutically, SKAT was preferred for SKAT responders and a vacuum suction pump (EHS) was used as a therapeutic option for non-responders. Other research groups even generally prefer the use of the vacuum pump [18]. Hauri [9] reported good success of arterial revascularization of penile gradients. However, because of the insufficient detection of vegetative neuropathies and the damage in the cavernous tissue demonstrated by light microscopy in patients with diabetes mellitus, other authors urge surgical restraint in this disease.

A compilation by Price et al. [18] criticized the current lack of information on erectile dysfunction treatment among both patients and physicians. Although most patients with erectile dysfunction wanted treatment, they rarely approached their primary care physician about the problem or received merely useless advice from their physician [12].

4.7 Scleroderma (progressive systemic sclerosis)

The occurrence of erectile dysfunction has also been reported in scleroderma, which belongs to the group of collagenoses [17]. Contrast cavities in the cavernosogram [18] and local accumulations of collagenous connective tissue [23] in the corpus cavernosum detectable by light microscopy suggest an organic cause in the sense of cavernous fibrosis. Because of the frequent occurrence of Raynaud's phenomenon in the hands of these patients, a secondary arteriopathy seems to be a relevant etiopathogenetic factor. Therapeutically, D-penicillamine and corticosteroids are used for the usually unfavorable course of the underlying disease, but little information is available on the value of this therapy in influencing erectile dysfunction. Isolated reports have been made of the difficult implantation of a penile prosthesis because of extensive cavernous fibrosis, and also of prosthesis removal because of postoperative glans necrosis [1]. In any case, interdisciplinary therapy planning with consideration of the overall prognosis seems reasonable.

Summary

Injuries to the penis or adjacent structures and diseases of the corpus cavernosum may be associated with erectile dysfunction. This must be considered during the history and clinical examination. Erectile dysfunction can also be a consequence of therapeutic interventions, and the patient must be informed of this preoperatively. In diabetes mellitus, erectile dysfunction must be expected to occur in every second patient during the disease.

Literature

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  2. Cytron S, Simon P, Segenreich E, Leib Z, Servadio C (1987) Changes in the sexual behavior of couples after prostatectomy - a prospective study. Eur Urol 13:35-38
  3. Eddi P, Ho PC, Bodenstab W, Parsons CL (1982) Erectile impotence associated with transurethral prostatectomy. Urology 19/3:259-262
  4. Fani K, Lundin AP et al (1983) Pathology of the penis in long term diabetic rats. Diabetologia 25:424-428
  5. Finkle AL, Prian DV (1966) Sexual potency in elderly men before and after prostatectomy. JAMA 196/2:125-129
  6. Gold FM, Hotchkiss RS (1969) Sexual potency following simple prostatectomy. NY State J Med 1:2987-2989
  7. Goldstein I, Feldman MI, Deckers PJ, Babayan RK, Krane RJ (1984) Radiation-associated impotence. JAMA 251:903-910
  8. Hargreve TB, Stephenson TP (1977) Potency and prostatectomy. Br J UroI 49:683-688
  9. Hauri D (1989) Operative Moglichkeiten in der Therapie der vascular bedingten erektilen Impotenz. Urologe A 5:260-264
  10. Holtgrewe HL, Valk WL (1964) Late results of transurethral prostatectomy. J Urol 92/1:51-55
  11. Jevtich MJ, Kass M, Khawand N (1985) Changes in the corpora cavernosa of impotent diabetics: comparing histological with clinical findings. J Urol (paris) 9115:281-285
  12. Levine FJ, Greenfield AJ, Goldstein I (1990) Arteriographically determined occlusive disease within the hypogastric-cavernous bed in impotent patients following blunt perineal and pelvic trauma. J Urol 144:1147-1153
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  16. Melman A (1988) Iatrogenic causes of erectile dysfunction. Urol Clin North Am 15/1:33-37
  17. Nowlin NS et al (1986) Impotence in scleroderma. Ann Intern Med 104:794-798
  18. Price DE et al (1991) Why are impotent diabetic men not being treated? Practical Diabetes 8/1:10-11 Literatur 77
  19. Rathert P (1981) Verletzungen der Genitalorgane. In: Lutzeyer W (Hrsg) Traumatologie des Urogenitaltraktes. Springer, Berlin Heidelberg New York Tokyo (Handbuch der Urologie, Bd 14, S 201-307)
  20. Schover LR (1987) Sexuality and fertility in urologic cancer patients. Cancer 60:553-558
  21. Sigel A, Chlepas S (1981) Verletzungen der Harnrlihre und der Harnblase. In: Lutzeyer W (Hrsg) Traumatologie des Urogenitaltraktes. Springer, Berlin Heiidelberg New York Tokyo (Handbuch der Urologie, Bd 14, S 131-199)
  22. Stelzner F (1977) Ober Potenzstlirungen nach Amputation und Kontinenzresektion des Rektums. Zentralbl Chir 102:212
  23. Sukenik S et al (1987) Impotence in systemic sclerosis. Ann Intern Med 106/6:910-911
  24. Thjada de S, Goldstein I, Azadzvi K, Krane RJ, Cohen MD (1989) Impaired neurogenic and endothelian-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med 320:1025-1030
  25. Thetter 0, Hochstetter A v, van Dongen RJAM (1984) Sexualfunktion nach gefaBchirurgischen Eingriffen im aortoiliacalen Bereich - Ursachen und Vermeidung von Potenzstlirungen
  26. Walsh PC, Mostwin JL (1984) Radical prostatectomy and cystoprostatectomy with preservation of potency: results using a new nerve sparing technique. Br J Urol 56:694
  27. Zohar J, Meiraz D, Maaz B, Durst N (1976) Factors influencing sexual activity after prostatectomy: a prospective study. J Urol 116:332-334
Author: S. Alloussi E. Becht H.-V. Braedel , D. Caspari Th. Gebhardt S. Meessen V. Moll , K. Schwerdtfeger J. Steffens
Source: Erektile Funktionsstorungen , Diagnostik, Therapie und Begutachtung