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Chapter 81: Erectile Dysfunction

INTRODUCTION

  • Erectile dysfunction (ED) is the persistent failure (minimum of 3 months) to achieve a penile erection suitable for sexual intercourse. Patients often refer to it as impotence.

PATHOPHYSIOLOGY

  • ED can result from any single abnormality or combination of abnormalities of the four systems necessary for a normal penile erection. Vascular, neurologic, or hormonal etiologies of ED are referred to as organic ED. Patients who do not respond to psychogenic stimuli and have no organic cause for dysfunction have psychogenic ED.

  • The penis has two corpora cavernosa and one corpus spongiosum, which contain interconnected sinuses that fill with blood to produce an erection that is sustained by occlusion of venous outflow from the corpora.

  • Acetylcholine works with other neurotransmitters (ie, cyclic guanylate monophosphate [cGMP], cyclic adenosine monophosphate [cAMP], or vasoactive intestinal po1ypeptide) to produce penile arterial vasodilation and ultimately an erection.

  • Organic ED is associated with diseases that compromise vascular flow to the corpora cavernosum (eg, peripheral vascular disease, arteriosclerosis, and essential hypertension), impair nerve conduction to the brain (eg, spinal cord injury and stroke), or impair peripheral nerve conduction (eg, diabetes mellitus). Secondary ED is associated with hypogonadism.

  • Psychogenic ED is associated with malaise, reactive depression or performance anxiety, sedation, Alzheimer disease, hypothyroidism, and mental disorders. Patients with psychogenic ED generally have a higher response rate to interventions than those with organic ED.

  • Social habits (eg, cigarette smoking and excessive ethanol intake) and medications (Table 81-1) can also cause ED.

TABLE 81-1Medication Classes That Can Cause Erectile Dysfunction
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TABLE 81-1 Medication Classes That Can Cause Erectile Dysfunction

Drug Class

Proposed Mechanism by Which Drug Causes Erectile Dysfunction

Special Notes

Anticholinergic agents (antihistamines, antiparkinsonian agents, tricyclic antidepressants, phenothiazines)

Anticholinergic activity

Second-generation nonsedating antihistamines (eg, loratadine, fexofenadine, or cetirizine) are associated with less erectile dysfunction than first-generation agents.

Selective serotonin reuptake inhibitor (SSRI) and multiple receptor reuptake inhibitor antidepressants cause less erectile dysfunction than tricyclic antidepressants. Of the SSRIs, paroxetine, sertraline, fluvoxamine, and fluoxetine cause erectile dysfunction more commonly than venlafaxine, nefazodone, trazodone, bupropion, duloxetine, mirtazapine, escitalopram, or vilazodone.

Phenothiazines with less anticholinergic effect (eg, chlorpromazine) can be substituted in some patients if erectile dysfunction is a problem.

Dopamine antagonists (eg, metoclopramide, phenothiazines)

Inhibit prolactin inhibitory factor, thereby increasing prolactin levels

Increased prolactin levels inhibit testicular testosterone production; depressed libido results.

Estrogens or drugs with antiandrogenic effects (eg, luteinizing hormone-releasing hormone superagonists, digoxin, spironolactone, ketoconazole, cimetidine)

Suppress testosterone-mediated stimulation of libido

In the face of a decreased libido, a secondary erectile dysfunction develops because of diminished sexual drive.

CNS depressants (eg, barbiturates, narcotics, benzodiazepines, short-term use of large doses of alcohol, anticonvulsants)

Suppress perception of psychogenic stimuli

Agents that decrease penile blood flow (eg, diuretics, peripheral β-adrenergic antagonists, or central sympatholytics [methyldopa, clonidine, guanethidine])

Reduce arteriolar flow to corpora

Any diuretic that produces a significant decrease in intravascular ...

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