INTRODUCTION AND OVERVIEW

Erectile dysfunction (ED) was defined by the 1992 National Institutes of Health Consensus Development Panel on Impotence as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual intercourse. It is a symptom that causes significant psychological and relationship stress and is often not investigated or treated, as a significant majority of men do not report it to their doctor.

Until the late 1980s, ED was regarded as mainly psychological in origin. We now understand that ED is a complex process requiring a combination of urological, endocrinological, psychological, vascular and biochemical factors for satisfactory function.

EPIDEMIOLOGY

In recent times there have been many epidemiological studies of erectile dysfunction, the hallmark study being the 1987 Massachusetts Male Aging Study.¹ This study found that ED occurred in 52% of men aged between 40 and 70 years. It confirmed that ED increases in frequency as men grow older, and that age is not a cause but an association of this condition. The study found that the most common pathological factor in ED is vascular disease, found in diabetes, hypertension, obesity and hyperlipidaemia (metabolic syndrome).

Thus the incidence of ED is highly correlated with health conditions such as metabolic syndrome, and with lifestyle factors such as smoking and lack of exercise.

The first Australian-based community study of ED was carried out by Chew and colleagues from the Keogh Institute for Medical Research, Perth, in 1997.² This study found that some degree of ED was present in almost 40% of men aged 18 years or older. Complete ED occurred in 18.6% of men. The prevalence of complete ED increased with age. Despite the frequency of ED, this study found that only 11.6% of men with ED had received treatment.

ANATOMY

The basic anatomy of the penis (Fig 49.1) consists of vascular cavernosal tissue that responds to neurological impulses, resulting in penile rigidity.

FIGURE 49.1 Basic anatomy of the penis

Each corpus cavernosum contains blood-filled compartments called sinusoids or lacunar spaces and is surrounded by a fibrous sheath called the tunica albuginea. The endothelium and integrity of the smooth muscle cells play an important role in the vascular events of erection.

The corpus spongiosum surrounds the urethra and distally forms the glans penis. The arterial inflow arises from the internal pudendal artery, which provides a cavernosal artery for each corpus.

Venous drainage occurs through emissary veins passing through the tunica albuginea. The rigidity during tumescence compresses these veins, causing veno-occlusion. When this mechanism functions poorly, it is often described as venous leakage.

Parasympathetic nerves from the S2 to S4 nerve root control erectile function, and sympathetic nerves from T11 to L2 control detumescence and ejaculation. Penile erection is thus a neurovascular event. Sexual stimulation results in increased parasympathetic activity, leading to release of neurotransmitters from the cavernous nerve terminals and relaxing factors from the endothelial cells in the penis. The neurotransmitters are acetylcholine, vasointestinal peptide and nitric oxide.

PATHOPHYSIOLOGY

Cyclic guanosine monophosphate (cGMP), which arises from the precursor L-arginine by the action of nitric oxide synthase, controls nitric oxide function. Calcium efflux mediated by cGMP leads to smooth muscle cell relaxation in the arteries and arterioles supplying the erectile tissue, increasing blood flow and causing the erection (Fig 49.2). This action is ended by phosphodiesterase type 5 (PDE-5), which leads to detumescence. Additional smooth muscle relaxation via the cyclic adenosine monophosphate (cAMP) pathway is mediated by prostaglandin E₁ and vasointestinal peptide. Availability of nitric oxide in the endothelium decreases with age. Endothelial dysfunction occurs in both coronary artery disease and ED when the action of nitric oxide is affected. Impaired nitric oxide synthesis reduces the capacity of vasodilation and increases the risk of platelet aggregation. Atherosclerosis has a greater effect in ED than the ageing process. Diabetes is associated with both vascular and neurological effects that interfere with the interaction between the endothelium and the smooth muscle cells.

FIGURE 49.2 Biochemical pathway of erection

AETIOLOGICAL FACTORS

As mentioned, the prevalence of ED increases with age; generally 70% of men at the age of 70 years describe a form of erectile dysfunction. Men with sexual dysfunction may have physical and psychological health problems (Box 49.1).

Psychological factors may be the primary cause of the ED or can arise secondary to the distress caused by its presence. Psychological factors include anxiety, stress, depression, relationship issues and other presentations of mental illness.

Erectile dysfunction may be associated with many medical conditions; it is strongly associated with atherosclerosis, making ED a marker of potential coronary artery disease. Because of the smaller size of the penile arteries compared to the coronary arteries, erectile dysfunction may precede coronary artery disease by 3–5 years. Thus a high level of total cholesterol with a low HDL is an important risk factor for ED causing both arterial and venous dysfunction due to endothelial injury and smooth muscle cell changes.

Smoking has been shown to be an important risk factor for ED. Smoking may result in the arterial inflow problems or faulty veno-occlusive mechanism. Obstructive sleep apnoea has been associated with reduced nocturnal erections.

Diabetes may involve vascular and neurological problems involving vascular insufficiency and sensory and autonomic neuropathy. Men with diabetes experience the onset of ED 10–15 years earlier than those without diabetes. More than 50% of these will have ED at some time, and 39% suffer from the condition all the time. The Massachusetts Male Aging Study showed a 28% probability of complete ED among men with diabetes, compared with a 9% probability in those without diabetes.¹ The risk may depend on the duration of diabetes and the presence of poor glycaemic control.

The neurological causes of ED include multiple sclerosis, temporal lobe epilepsy, Parkinson’s disease, stroke, Alzheimer’s disease and spinal cord injury. Hypoxia associated with respiratory disease may result in the aggravating vascular causes of ED. Renal insufficiency may result in ED in up to 50% of patients due to multiple causes, including vascular, neurological, endocrine and electrolyte and mineral issues.