Indian Write- Ups

Management
Erectile Dysfunction In Diabetics

Dr. Nilanjan Sengupta MD, Dr. Subhankar Chowdhury, DTM & H, MD, DM, MRCP Dept. of

Endocrinology & Metabolism, IPGMER & SSKM Hospital, Kolkata.


 
Impotence or erectile dysfunction (ED) is a common, but often neglected complication of diabetes mellitus. Patients often suffer silently but are ashamed of communicating their problem to physician. The busy practitioner, on the other hand, may not have the time to elicit a detailed sexual history from every diabetic patient that he encounters. But loss of erectile capacity may have a debilitating psychological effect on the patient and can disrupt conjugal relationships. The reported prevalence of ED in diabetic men has ranged from 35-75%.
 
The age old term "impotence" derived from Latin impotentia, meaning "lack of strength" has been replaced by the term erectile dysfunction in view of the stigma attached to the former.
 
Definition
 
The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM IV) of the American Psychiatric Association describes ED as a persistent or recurrent inability to attain an adequate erection or to maintain the same until completion of sexual activity.
 
Physiology
 
Erection is a neurovascular phenomenon under psychogenic control. An inflow of blood into the corpora cavernosa with prevention of regress of the same results in penile tumescene and erection. This cavernosal vasodilatation is brought about by stimulation of parasympathetic nerves (S2-S4). Various neurotransmitters are involved in the erectile process but nitric oxide (NO) is of supreme importance. The postganglionic parasympathetic nerve fibres innervating the cavernosal arteries release NO, which helps in the formation of cyclic guanosine monophosphate (cGMP) that ultimately results in smooth muscle relaxation and vasodilatation, cGMP is degraded by phosphodiesterases (PDE), especially isoenzymes 5 and 6.
 
Causes
 
A majority of ED in diabetics has an organic basis and is commonly the result of penile autonomic neuropathy, cavernosal arterial insufficiency, consequent on atherosclerosis, or defective corporal veno-occlusive mechanism. However, in particular case the aetiology may be multifactorial and there is no reason why a diabetic patient cannot have ED due to other causes viz. psychogenic ED, hypogonadism, hyperprolactinaemia, substance abuse and drug induced ED (as for instance, caused by antipsychotics, anti-depressants and alpha methyl dopa). Though in most cases ED in diabetics is not self-limited, poor glycaemic control can cause a reversible ED, primarily by reducing libido.
 
Diagnostic Evaluation
 
Nocturnal penile tumescence (NPT): To decide whether a case of ED is organic or functional, assessment of NPT is the best since the 2-4 episodes of erection that occur in association with rapid eye movement (REM) sleep are not putatively subject to psychogenic inhibition.
 
In the Stamp test or snap gauge test for NPT, the flaccid penis has a string of stamps or a ring placed around it at bedtime. A snap in the string of stamps or a broken ring in the morning indicates NPT. In a sleep laboratory, the penile circumference can be monitored continuously using sophisticated instruments like Rigiscan. However, the recent evidences pointing to the fact that the patient’s history of nocturnal and morning erections corresponds well to NPT is supportive of the view to rely on the patient’s history alone on most occasions rather than to go in for these tests.
 
Visual sexual stimulation test: It utilizes video-taped erotic material in a laboratory setting to monitor erection by strain gauge.
 
Penile brachia pressure index (PBPI): This is the ratio between the brachial and penile systolic blood pressures. The penile blood pressure is measured by a hand-held Doppler instrument using a neonatal sphygmomanometer cuff. A PBPI exceeding 0.75 excludes vasculogenic ED whereas a value less that 0.65 suggests vascular abnormality.
 
Penile duplex ultra-sonography: This helps to determine the peak systolic cavernosal arterial blood flow both in the flaccid state and after administration of a vasodilator intracaversonally. A low flow velocity is indicative of arterial in insufficiency.
 
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