In the second case, a supra-pubic prostatectomy, there was sufficient post surgical symptomatology to stimulate onset of symptoms of secondary impotence. In this situation the untoward surgical result was unfortunate. The distress in both instances was that the men had not been forewarned of the possible side effects of the surgery.
The case of secondary impotence developing after the supra-pubic prostatectomy was brought under control during therapy.
Prostatic cancer patients:
Those facing surgery, should be made aware by the operating surgeon that the loss of erective function can and does accompany such surgery. The psychosexual trauma forced upon the postoperative patient and his wife because they were not informed before surgery of the resultant sexual dysfunction is unforgivable.
The physiological influence of diabetes on secondary impotence is in a special category. In 6 of the total of 9 cases the onset of secondary impotence had been associated with the diabetes by consultative authority prior to referral for therapy, while in the remaining 3 instances no correlation between the established clinical condition of diabetes and the onset of impotence had been suggested by referring professionals.
Additionally, in 11cases of referral for secondary impotence without concept of etiological influence clinical diabetes (3 cases) and preclinical diabetes (8 cases) were diagnosed during metabolic work-ups that are part of the routine physical and laboratory evaluations of the secondarily impotent male referred for diagnosis and treatment.
As described in therapy treatments, a routine five-hour glucose-tolerance test is conducted for men referred for secondary impotence. This evaluation technique has been in effect for five years but has not reached the stage of statistical significance.
This work will be reported as a separate entity in monograph form at a later date. The statistical evaluation suggests that there is a 200-300 percent higher incidence of a diabetic or prediabetic curve reported for men with the clinical symptoms of secondary impotence, when returns are compared to the incidence of diabetic or prediabetic curves in similar glucose-tolerance testing of a representative cross-section of the population.
There is no supportable concept at this time that diabetes is an associate of equality with other etiological influences on secondary impotence. Nor does this work imply that the diabetic male has an established predisposition toward impotence. The amount of information available currently does not allow a firm clinical position.
Of course, there frequently are other etiological foci to combine with a diabetic or prediabetic state to influence the onset of secondary impotence. However, if a man is referred for secondary impotence, evaluation of his diabetic status should be a routine part of the total physical and laboratory work up.
It should be emphasized in context that even if symptoms of secondary impotence represent an end-point of etiological influence from a diabetic or prediabetic state, adequate institution and careful maintenance of medical control of the diabetes will not reverse the symptoms of impotence, once developed.
Difficulty lies, of course, in the fact that regardless of etiology, once lack of erective security has been established, fears of performance unalterably become an integral part of the psychosocial influences of the man's daily life. Adequate medical control of the diabetes will provide no relief for his fears for sexual performance.
If diabetes or a prediabetic state can influence the onset of secondary impotence in other than advanced states of diabetic neuropathy, this fact is but another example of the multiple etiological aspects of secondary impotence.
Understandably, for many years the pattern of the human male has been to blame sexual dysfunction on specific physical distresses.
Every sexually inadequate male lunges toward any potential physical excuse for sexual malfunction. From point of ego support, would that it could be true.
A cast for a leg or a sling for an arm provides socially acceptable evidence of physical dysfunction of these extremities. Unfortunately the psychosocial causes of perpetual penile flaccidity cannot be explained or excused by devices for mechanical support.