The anorectum

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17 The anorectum

Applied surgical anatomy

The anus enables the passage of stool or flatus (when socially convenient) but is also capable of maintaining continence to gas, fluid and solid at almost all other times in healthy individuals.

Anal musculature and innervation

The anal canal is 3–4 cm long in males and slightly shorter in females. It consists of two concentric muscle layers known as the internal and external sphincters (Fig. 17.1). The internal sphincter is a condensation of the circular smooth muscle of the rectum and is a continuation of the circular muscle of the gastrointestinal tract. It is controlled by the autonomic nervous system with fibres from the pelvic sympathetic nerves, the lower lumbar ganglia and the pre-aortic/inferior mesenteric plexus. Parasympathetic fibres arise from the sacral plexus. The smooth muscle of the internal sphincter maintains tone and contributes to resting pressure within the anal canal, so playing an important role in maintaining continence. The longitudinal muscle of the gut ends at the anus as a series of fibrous bands that radiate to the perianal skin, and is of little consequence to perianal disease. The striated muscle of the external sphincter is under voluntary control, being innervated bilaterally by the internal pudendal nerves and the fourth branch of the sacral plexus. The circular muscle tube of the external sphincter blends with the lower part of the levator ani, known as the puborectalis sling (Fig. 17.2). The puborectalis fibres of the levator ani originate from the posterior aspect of the pubic symphysis and pass posteriorly to join the external sphincter. The levator ani muscles themselves are also important in maintaining the relationship of the anus and rectum during defaecation.

Anal canal epithelium

The cell type of the anal canal epithelium determines why certain diseases, such as tumours and viral infections, affect only particular levels of the canal. The epithelium of the anal canal is specialized and contains three distinct zones. The external zone (from dentate line to anal verge) is keratinized, stratified squamous epithelium. There is a short, modified, anal transitional zone of non-keratinized squamous epithelium, which lies immediately proximal to the dentate line, separated from the columnar epithelial of the anal canal but continuous with the rectal epithelium. The anal valves are crescentic mucosal folds that form a serrated or dentate line on the luminal aspect of the mid-anal canal (Fig. 17.3). The dentate line represents the line of fusion between the endoderm of the embryonic hindgut and the ectoderm of the anal pit. Thus, the epithelium is innervated by the autonomic nervous system and is insensate with respect to somatic sensation. The canal lining below the dentate line is innervated by the peripheral nervous system and so conditions affecting this region, such as abscess, anal fissure or tumour, result in anal pain.

The composition of the epithelium of the anorectum determines the type of tumour that affects the region. Thus, squamous cell carcinoma of the anal canal arises from the epithelium below the dentate line or in the transitional zone of non-keratinized squamous epithelium. Because the canal above the anal transition zone contains columnar glandular epithelium, tumours of the upper anal canal are adenocarcinoma; they are best considered as a low rectal cancer and treated accordingly.

There are 4–8 specialized anal glands located within the substance of the internal sphincter or in the space between the internal and external sphincters at the level of the mid-anal canal; these glands have ducts that open directly on to the dentate line (Fig. 17.4). They are involved in the aetiology of perianal abscess and fistula-in-ano. The function of the anal glands is to secrete mucus, lubricating and protecting the delicate epithelium of the anal transition zone. The ducts from these glands open into the folds of mucosa at the dentate line. The relevance of these glands lies in the fact that they are the source of most perianal abscesses. When an anal gland duct becomes occluded, the obstructed gland may become infected with gut organisms such as coliforms, and anaerobic bacteria such as Bacteroides.

Anorectal disorders

Haemorrhoids

Despite haemorrhoids (colloquially known as piles) being very common, the aetiology remains obscure. Almost all haemorrhoids are primary, with only a tiny proportion due to other factors, such as a cancer in the distal rectum. Haemorrhoids are enlarged, prolapsed anal cushions and the pathophysiology involves degeneration of the supporting fibroelastic tissue and smooth muscle, with enlargement and protrusion of the cushions at the 3, 7 and 11 o’clock position. As the cushions prolapse, there is keratinization and hypertrophy of the overlying anal transitional zone and eventually prolapse of the columnar epithelial component in advanced stages. However, the underlying cause of the stretching of the fibroelastic support is unknown. Constipation and straining at stool are common features. These may be aggravated by a high anal sphincter pressure, with further entrapment of prolapsed piles. Haemorrhoids during pregnancy are very common and are probably due to hormonal effects inducing connective tissue laxity, combined with constipation and pressure from the baby’s head. Sitting on the toilet for long periods, such as when reading, is also held to be an associated aetiological factor. However, as with other putative aetiological factors, there is no real evidence for cause and effect.

Clinical features

Bleeding and prolapse are the cardinal features and may occur in isolation or together. The bleeding is typically intermittent ‘outlet-type’ bleeding, separate from the stool and evident in the pan or only on wiping. There may also be aching or dragging discomfort on defaecation, and patients may self-reduce their piles to obtain relief after each bowel motion. Severe constant pain is unusual and in such cases other pathology should be suspected. In the later stages, haemorrhoids remain prolapsed at all times and there is staining of the underwear with mucus and faecal fluid. However, it is very unusual for patients to present with incontinence of solid faeces and a sphincter defect should be suspected in such cases. In cases of constant prolapse, there is often pruritus due to the discharge, with irritation of the perianal skin.

Haemorrhoids can be staged according to the degree of prolapse, but it is important to note that this classification does not necessarily relate to the amount of trouble that symptoms cause the patient:

Patients may present as an emergency with a complication of haemorrhoids, such as thrombosed prolapsed piles or torrential haemorrhage. Prolapsing haemorrhoids may acutely thrombose and there is associated marked sphincter spasm. The thrombosed piles are large, swollen, irreducible haemorrhoids, which are dark blue or even black owing to necrosis and submucosal haemorrhage. They are acutely painful and tender and the diagnosis is easily made on inspection, but a rectal examination will be impossible because of pain. Major haemorrhage, resulting in significant hypovolaemia and anaemia, is unusual but should be excluded in any patient presenting with a major fresh rectal bleed.

Management

In many cases, reassurance after appropriate evaluation is all that many patients require. Specific treatment is not required for most cases, as symptoms are minor and intermittent. A high-fibre diet with plenty of vegetables is commonly recommended, although there is no good evidence that this actually provides any benefit at all. However, if constipation is a feature, it does seem reasonable advice; in some cases, bulk laxatives or stool softeners may be indicated. Patients often self-medicate with proprietary ointments and creams. There is no good evidence from controlled trials that these are effective, but if patients find that they help, then it seems reasonable to advise their intermittent use.

Operative approaches

The principle of haemorrhoidectomy involves total removal of the haemorrhoidal mass and securing of haemostasis of the feeding vessel. The wound can be left open or can be closed, but there are rarely problems with healing or infection. In some cases, there are secondary haemorrhoids between the main right anterior, right posterior and left lateral positions, and these are also removed as part of the operation. Recently, a different surgical approach using a circular stapler has been developed, the stapled anopexy. This technique aims to divide the mucosa and haemorrhoidal cushions above the dentate line in order to transect the feeding vessels and hitch up the stretched supporting fibroelastic tissue, rather than removing the whole haemorrhoidal mass as in the standard haemorrhoidectomy. Stapled haemorrhoidectomy may have a place for the treatment of symptomatic first- and second-degree piles (EBM 17.1). With all surgical approaches to treating

piles, it is important to consider that the haemorrhoidal cushions contribute to fine control of continence. Hence, an element of anal incontinence can be one of the long-term sequelae of any haemorrhoidectomy. Surgery should not be considered lightly.

Fissure-in-ano

Fissure-in-ano is a common condition characterized by a linear anal ulcer, often with the internal sphincter visible in the base, affecting the anal canal below the dentate line from the anal transition zone to the anal verge (Fig. 17.7). There is often little in the way of granulation tissue in the ulcer base. Owing to failed attempts at healing, there may be a tag of skin at the lowermost extent of the fissure, known as a ‘sentinel pile’. At the proximal extent of the fissure there may be a hypertrophied anal papilla. Sometimes fissures will heal incompletely and mucosa will bridge the edges of the fissure. This results in a low perianal fistula and may present years later. Fissures are most frequently observed in the posterior midline of the anal canal, although anterior fissures may occur in women following childbirth; they are rarely seen in males.

The condition most commonly affects people in their twenties and thirties, with a slight male preponderance. Most fissures are idiopathic, but it is clear that the pathophysiology involves ischaemia in the base of the ulcer, associated with marked anal spasm and a significantly raised resting anal pressure. Successive bowel motions provoke further trauma, pain and anal spasm, resulting in a vicious circle of anal pain and sphincter spasm that causes further trauma to the anal mucosa during defaecation. Fissures may be acute and settle spontaneously, but chronic anal fissure is defined as an ulcer that has been present for at least 6 weeks. Recurrent multiple or unusually extensive fissures affecting areas other than the midline should raise the suspicion of Crohn’s disease, which can occasionally present with anal fissure as the sole initial complaint. Occasionally, anal fissure may be associated with ulcerative colitis. Fissure is an uncommon complication of haemorrhoidectomy and results from a non-healing wound combined with anal spasm.

Fissure-in-ano is one of the most common causes of constipation in infants and children. The pain associated with the fissure leads to a pattern of behaviour in which the child tries to avoid defaecation. This results in stool retention and rectal stool bolus formation. The rectum becomes overdistended and the child becomes unaware of the need to pass stool. Overflow incontinence and soiling result.

Management

Many acute fissures resolve spontaneously and so treatment should be reserved for chronic symptoms of 6 weeks’ or more duration. Having established that the fissure is primary, treatment is aimed at alleviating pain and anal spasm in order to break out of the vicious circle. It is important to document reproductive history for females, as surgery may have implications for future anal continence.

The optimal approach is conservative in the first instance. Stool softeners may help, but rarely effect a cure as the sole treatment. Chemical sphincter relaxation is first-line treatment of choice using topical 0.5% diltiazem or nitrates (glyceryl trinitrate 0.2–0.5%) as a cream applied 12-hourly to the anal canal. Headaches can be a dose-limiting side effect especially with topical nitrates, but healing can be achieved in 50–70% of chronic fissures. Other means of reduction in sphincter tone include direct injection of the sphincter with botulinum toxin, which temporarily paralyses the sphincter.

Until the relatively recent advent of chemical sphincterotomy as first-line treatment, surgery was the only option. Surgery still has a major role in the management of patients who have fissures resistant to medical treatment, or who have recurrence. Anal stretching has been abandoned, as it is associated with significant sphincter damage and the risk of incontinence (EBM 17.2). Lateral sphincterotomy is the most common operation for anal fissure and involves controlled division of the lower half of the internal sphincter at the lateral position (3 o’clock or 9 o’clock with the patient in the lithotomy position). There is a small but appreciable risk of late anal incontinence following lateral sphincterotomy. This is usually only to gas, but occasionally faecal incontinence to liquid or solid can occur, particularly in women who have had birth-related anal sphincter damage. In women, it may therefore be more appropriate to avoid further division of any sphincter muscle, and this can be achieved using an anal advancement flap or a rotation flap to cover the ulcerated base of the fissure and allow new, well-vascularized skin to heal the ulcer and reduce the associated anal spasm.

Perianal abscess

Perianal abscess is a nonspecific term encompassing abscesses in the perianal, intersphincteric, ischiorectal or pelvirectal spaces (Fig. 17.8). Perianal suppuration is common, affecting men three times more frequently than women.

Conditions that predispose to perianal abscess include Crohn’s disease and ulcerative colitis, as well as any cause of immunosuppression such as haematological disease, diabetes mellitus, chemotherapy and human immunodeficiency virus (HIV) infection. Most patients who present with perianal abscess have no predisposing factors and most abscesses are cryptoglandular, initiated by blockage of the anal gland ducts (see Fig. 17.3). The obstructed anal gland becomes secondarily infected with large bowel organisms such as Bacteroides, Streptococcus faecalis and coliforms. The fact that the anal glands are situated in the intersphincteric space (see Fig. 17.4) explains the routes that the infection may take as pus tracks along the line of least resistance through the tissue spaces. Rarely, patients with established sepsis elsewhere may develop metastatic suppuration in the perianal region.

Clinical features

In cases where the abscess remains localized within the intersphincteric space, the patient presents with acute anal pain and tenderness. There is usually no evidence of suppuration on inspection of the perianal region. Pain often prevents digital examination, and so general anaesthetic is required. The main differential diagnosis is acute anal fissure. The diagnosis is confirmed by demonstration of a localized pea-sized lump in the intersphincteric space. True perianal abscess is the most common type, in which pus tracks inferiorly to appear at the perianal margin between the internal and external sphincters (Fig. 17.8). Symptoms are usually of 2–3 days’ duration and the abscess may have discharged spontaneously. Systemic upset is minimal and anal pain is the predominant presenting complaint.

Infection may extend into the ischiorectal space resulting in ischiorectal abscess, which is a relatively uncommon but serious problem. Poorly controlled diabetes is a common underlying correlate and should be excluded in all cases. As the ischiorectal space is horseshoe-shaped and there are no fascial barriers within it, infection can track extensively, including posteriorly around the anus to affect the contra-lateral space. In such cases, the patient is toxic and pyrexial with a large, painful, fluctuant, brawny swelling affecting both buttocks, due to large volumes of pus. There is a history of perianal pain for several days, associated with difficulty in sitting.

Infection tracking upwards from the infected anal gland through the upper part of the intersphincteric space may result in a high intersphincteric (high intermuscular) abscess or a pelvirectal abscess. As these spaces encircle the anorectum above the levator muscles, abscesses can be bilateral and often present with a major systemic upset. These are complex problems meriting specialist management. With high abscesses, it is also important to consider intra-abdominal sepsis from Crohn’s or diverticular abscess.

Management

An established abscess will not respond to antibiotics alone and requires surgical drainage. Treatment of perianal abscess is usually straightforward and involves drainage of the pus under general anaesthetic. Most cases are adequately dealt with by incising and deroofing the abscess at the point of maximal fluctuance. However, anatomical considerations are important, as inappropriate incision of sphincter muscle can result in incontinence in the long term. Furthermore, drainage of pus through the wrong space will create a perianal fistula (see below). At operation, pus should be sent for bacteriological assessment to determine the causative organism(s). In uncomplicated cases, antibiotics have no place after incision and drainage. Where there is extensive cellulitis, as is often the case with ischiorectal abscess, parenteral antibiotics, such as broad-spectrum cephalosporins and metronidazole, should be administered. Parenteral antibiotics are mandatory for diabetic patients with peri-anal sepsis. Unusually complex perianal sepsis or recurrent abscess should raise suspicion of underlying Crohn’s disease. Sigmoidoscopy and rectal biopsy should be performed and the roof of the abscess sent for histology.

Fistula-in-ano

The underlying pathogenesis of the vast majority of cases of perianal abscess or anal fistula is obstruction of the anal gland duct. This results in stasis and infection of the anal gland (cryptoglandular infection). Abscess precedes all such cases of fistula, although the sepsis is often subclinical. Inappropriate surgical drainage of perianal abscess is responsible for a small but significant proportion of fistulae. Figure 17.9 is a simplified diagram showing the classification of fistula-in-ano. A fistulous tract should be suspected in all patients with recurrent perianal abscess. Typically the patient presents repeatedly with an abscess that intermittently points and discharges pus on to the perianal skin. However, there is no need to search routinely for a fistula when draining straightforward perianal abscesses. Inexpert probing may inadvertently induce a fistula.

In addition to cryptoglandular aetiology, perianal fistula may be due to Crohn’s disease, anal trauma, inexpert surgical drainage and anorectal carcinoma. Other rare causes include ulcerative colitis, tuberculosis and actinomycosis. Around 10% of patients with small intestinal Crohn’s disease without colorectal involvement, have perianal disease. Hence, it is important to exclude Crohn’s disease in patients with recurrent perianal fistula or sepsis resistant to treatment.

Clinical features and assessment

In most cases, the patient presents with a chronically discharging opening in the perianal skin, associated with pruritus and perianal discomfort. A detailed clinical history is essential to determine any predisposing medical conditions or previous surgery. Investigation requires examination under anaesthetic (EUA) by a colorectal specialist when the fistula should be probed to trace the tract from external to the internal openings. Goodsall’s Law is a rough rule of thumb as to the likely course of fistulous tracts. Thus, when the fistula opens on the perianal skin of the anterior anus, the tract usually passes radially directly to the anal canal. However, when the opening is posterior to a line drawn between the 3 o’clock and 9 o’clock positions (Fig. 17.10), then the tract usually passes circumferentially backwards and enters the anal canal in the midline (6 o’clock position). It is essential to avoid inducing further fistulae by ill-advised probing of the region. It is important to determine whether the fistula is low or high (Fig. 17.9), as the prognosis and treatment are different for each. Most fistulae can be delineated and treated at EUA, but complex cases may merit magnetic resonance imaging (MRI). MRI of a complex high fistula involving the pelvirectal space is shown in Figure 17.11. Endoanal ultrasound may be useful. Further investigation to exclude Crohn’s disease may be appropriate, involving colonoscopy, small bowel MRI or small bowel follow-through.

Management

Treatment is determined by the course of the fistula tract. Usually, low fistulae can simply be laid open and allowed to heal. However, where a significant proportion of the internal and/or external sphincter is involved, then laying open the tract will result in faecal incontinence. In such complex cases, the fistula tract can be probed and a seton passed along its length (Fig. 17.12) to allow the fistula to drain. Once it is drained, a tighter seton can be applied that will gradually cut out through the sphincters, allowing them to heal behind the seton. Applying such a cutting seton maintains the ends of the sphincters together and minimizes the risk of incontinence. High fistulae may be treated by an anorectal advancement flap. This involves raising a flap of rectal wall and upper internal sphincter. The flap is advanced distally to close the internal opening. The external opening and superficial part of the tract heals as there is no faecal stream to maintain the sepsis. In some complex cases, a defunctioning colostomy may be necessary.

Miscellaneous benign perianal lumps

Anal cancer

Anal cancer is rare in comparison with colorectal cancer. There are around 600 new cases annually in the UK. Over 85% of anal cancers are squamous in origin and arise from the keratinized squamous epithelium of the anal margin or from the non-keratinized squamous epithelium of the anal transitional zone immediately above the dentate line. Anal verge tumours often present earlier than canal tumours because the patient becomes aware of a mass or irregular area at the anal margin. Around 5% of tumours are adenocarcinomas and these arise from the glandular epithelium of the upper anal canal or rarely from the anal glands located in the intersphincteric space. These are distinct from low anorectal adenocarcinoma. Most patients with anal cancer present in the sixth or seventh decade, but younger cases are well recognized, particularly in those with HIV and high risk activities. Other rarer tumours include melanoma, lymphoma and sarcoma.

There is a strong association between anal cancer and infection with HPV types 16 and 18. HPV infection is responsible for the majority of anal carcinomas. Smoking is a risk factor and likely interacts with viral infection. Anogenital warts are also a risk factor, as is anoreceptive intercourse. HIV infection is also a predisposing factor, owing to im-munosuppression and susceptibility to viral infection. The premalignant lesion, anal intraepithelial neoplasia (AIN), is probably the precursor of most anal carcinomas and is analogous to cervical intraepithelial neoplasia (CIN), the precursor lesion of cervical cancer. The level of AIN (1–3) is dependent on the degree of cytological atypia and the depth of that atypia in the epidermis. A high proportion of AIN 3 progresses to carcinoma and is shown in Figure 17.13. It is important to perform a cervical smear in patients with proven anal cancer. There is also an association with vulval intraepithelial neoplasia (VIN), which also has a common HPV aetiology.

Staging

Staging is important for prognosis and also guides treatment approaches. The TNM staging system for anal cancer is shown in Table 17.1. The lymph nodes most commonly involved are the inguinal groups, particularly for anal verge cancers. Canal tumours may spread proximally to the mesorectal nodes or to the internal iliac nodes via the middle rectal lymph nodes. Lymphadenopathy alone is not sufficient to confirm lymph node spread, and accessible nodes should be biopsied because reactive changes due to infection are common. Examination under anaesthetic is an important part of clinical staging, as the tumour is often painful and the anus tender to digital examination. CT and MRI are essential; endoanal ultrasound may be helpful but usually needs to be performed under anaesthetic.

Table 17.1 TNM staging of anal cancer

T (Tumour)

N (node)

M (Metastases)

Management

It is important to detect anal cancer at an early stage, as extensive local invasion and metastatic disease are associated with a poor outcome. Multidisciplinary treatment of anal cancer is essential with surgeon and radiotherapist involved in assessment and treatment.

For early, well-circumscribed superficial (T1N0) carcinomas, wide surgical excision is the optimal treatment, as it avoids the morbidity of chemoradiotherapy. However, for T2, T3 and T4 tumours, treatment comprises radiotherapy to the anal canal and inguinal lymph nodes, combined with 5-fluorouracil (5-FU) (recently capecitabine is preferred) and mitomycin C (EBM 17.3). Newer regimens of radiotherapy, combined with capecitabine and cisplatinum, are also being introduced. The usual approach is external beam radiotherapy, but radioactive implants such as selectron wires are also used in selected cases. Surgery has a limited role in the primary treatment of these lesions but does play an important part in the management of advanced disease. Surgery is reserved for radiotherapy treatment failures, when ‘salvage’ abdominoperineal excision of the anus and rectum may afford a cure in some cases and alleviate symptoms in others.

Modern multimodality approaches involving tailored surgery and chemoradiation have radically improved the morbidity of treatment by avoiding abdominoperineal resection and permanent colostomy for many patients; the 5-year survival rate is now around 65%.

Rectal prolapse

Rectal prolapse is a distressing condition that can affect young and older adults, as well as children. The term rectal prolapse encompasses three types of abnormal protrusion of all, or part of, the rectal wall:

The pathological process that results in rectal prolapse is incompletely understood. However, certain factors are clearly implicated in predisposing to the condition. Mucosal prolapse should not be confused with full-thickness prolapse. It is often associated with a degree of haemorrhoids, but whether these are causal or simply the result of a common aetiology is not understood. The majority of cases of full-thickness rectal prolapse occur in elderly women, with no obvious aetiological basis. Weight loss in the elderly with loss of fat supporting the rectum, combined with degeneration of collagen fibres and weakness of the musculature of the pelvic floor, results in loss of the anorectal angle and laxity of the rectal wall (see Fig. 17.2). In many cases, there is a deep rectovaginal pouch with a long loop of sigmoid colon that pushes down into the rectovaginal pouch and contributes to the prolapse. Occasionally, there is a clear history of obstetric injury but most patients are nulliparous.

Chronic constipation and straining at stool are the most common aetiological factors in young adults, although spinal injury, psychiatric illness, multiple sclerosis, spinal injuries and spinal tumour are predisposing factors. In children, the lack of a sacral hollow, combined with constipation and excessive straining at stool, is responsible for evagination of the rectum and protrusion of the prolapse through the anus. In children with cystic fibrosis, excessive coughing contributes to elevated intra-abdominal pressure.

Clinical features and assessment

Patients present with an uncomfortable sensation of ‘something coming down’ the back passage. Initially, this is only on defaecation, but eventually the rectum remains constantly prolapsed and will not reduce spontaneously. The patient may be able to reduce the prolapse digitally. Constipation is usually an accompanying feature. There is often a degree of faecal incontinence and there may be mucous discharge into the underwear. Blood-stained mucus is also common when the rectum remains prolapsed. The prolapse may become ulcerated and may become strangulated. In extreme cases, there may be associated uterine prolapse, alluding to the fact that the underlying aetiology relates to weakness of the entire pelvic floor.

Examination confirms the diagnosis in most cases. If the prolapse is not apparent, it will usually appear when the patient strains on a commode. A typical example of a full-thickness rectal prolapse is shown in Figure 17.15. Digital examination reveals a patulous anus, poor sphincter tone and evidence of a weak pelvic floor on straining. Rigid sigmoidoscopy will reveal cases of occult prolapse. If the history is of short duration, consideration should be given to the presence of a spinal tumour, a spinal stenosis or a prolapsed intervertebral disc. In occult rectal prolapse, radiological assessment using a defaecating proctogram or dynamic MRI may help secure the diagnosis. Conditions that might be mistaken for a rectal prolapse include large fourth-degree haemorrhoids, prolapsing rectal neoplasia, anal warts, anal skin tags and fibroepithelial anal polyp. On the basis of symptoms alone, the differential diagnosis of rectal prolapse includes rectal cancer and inflammatory bowel disease, and these should be excluded by appropriate investigations.

Management

Anal incontinence

Several factors are involved in maintaining anal continence (see Box 17.1) and these may be adversely affected by any combination of structural damage to the musculature, disruption of the nerve supply, and marked intestinal hurry with defaecatory urgency (such as in ulcerative colitis). Damage to the internal or external sphincters may occur during childbirth. Peripartum nerve injury due to a prolonged 2nd stage of delivery due to pressure effects from the baby’s head or due to forceps can affect the pudendal nerves, eventually leading to denervation and atrophy of the striated muscle of the external sphincter, the puborectalis sling and the levator ani. Neurodegenerative disease is also a recognized aetiological factor. Perianal sepsis or the surgery required to treat it, may result in structural damage to the sphincter complex.

Faecal incontinence is both distressing and socially disabling, but patients are often reluctant to discuss the issue with relatives or with medical professionals due to social stigma and embarrassment. Hence, the population prevalence of incontinence is probably underestimated. Nevertheless, it has been variously estimated at 2–5% in the general population and 10% of adult females. There are a variety of specific aetiological factors but the majority of cases are ‘idiopathic’, most commonly affecting older parous women. Aetiological factors associated with anal incontinence are listed in Table 17.2.

Table 17.2 Aetiology of anal incontinence

Trauma

Congenital

Neurological

Miscellaneous

The majority of patients are women with a past history of obstetric problems and difficult deliveries. The underlying mechanism of subsequent incontinence in such cases is complex. Although full-thickness obstetric tears are rare, significant sphincter defects have been observed to occur in 10–30% of women after vaginal delivery. As well as structural sphincter defects, prolonged labour may lead to internal pudendal nerve damage. Denervation of the pelvic floor results in atrophy of the sphincter complex and the levator ani in later life. Most cases of incontinence involve a combination of sphincter muscle damage and the secondary effects of denervation.

Clinical features and assessment

A full history is essential, with particular reference to obstetric history and any past perianal operations. Incontinence should be graded using established scoring systems, such as the Cleveland Clinic Incontinence Score, which incorporate frequency and severity of episodes of incontinence to gas, liquid or solid stool. Such scores enable more objective assessment of any improvement or deterioration in incontinence. Coexisting disease should be documented and neurological symptoms sought. A defaecation history should be sought, including the degree of defaecatory urgency. It is important to enquire about co-existing urinary incontinence. Examination to determine sphincter tone, the presence of previous scars and the state of the rectovaginal septum should be undertaken. Poor anal sensation suggests a neurogenic basis for the incontinence. Other anorectal causes of incontinence, as listed in Table 17.2, should be excluded where possible, and by rigid sigmoidoscopy in all cases. It is important to remember that any cause of intestinal hurry (such as colonic cancer, inflammatory bowel disease or even infective diarrhoea) can render incontinent a patient who had previously been coping with a more formed stool. Hence, colonoscopy is an important part of assessment. Endoanal ultrasound scanning of the sphincters delineates the presence and extent of any sphincter defect. Anorectal physiology studies document resting and squeeze anal sphincter pressures, and also define whether there is a predominant neurogenic element. Where there is any concern from the history or clinical examination regarding a spinal lesion, MRI should be performed.

Conservative management

Any remedial causes of incontinence (Table 17.2) should be addressed appropriately. However, women with ‘idiopathic’ faecal incontinence constitute the majority of cases. In older women, who almost universally have a combination of sphincter and nerve damage, conservative measures should be instigated in the first instance. Dietary advice is important to avoid exacerbating factors in the diet, such as caffeine, spicy foods and excessive alcohol. Stool-bulking agents such as Fybogel should be combined with loperamide to reduce the propulsive activity of the GI tract and induce a degree of constipation. In cases with a predominant neurogenic basis, rectal irritability resulting in faecal urgency may respond to therapy with amitriptyline (25–50 mg at night). Conservative measures should be combined with regular emptying of the rectum using stimulant suppositories or enemas. In many cases, these measures have a dramatic beneficial effect on quality of life even when minor degrees of incontinence persist.

Surgical management

Surgery is indicated only in a small minority of patients with idiopathic faecal incontinence. In a small subset of patients with a clear history of sphincter injury due to trauma or to surgical injury, overlapping sphincter repair is frequently highly successful. However, it is important to underline that overall the results of anterior sphincter repair are poor in the long term. Patients with evidence of denervation tend to have poor results. Complex total floor repairs have been performed with some success in a limited proportion of patients. Other surgical approaches include stimulated graciloplasty – transferring the gracilis muscle on a proximal pedicle to wrap it subcutaneously around the anal canal. An electrical stimulator is implanted, which delivers an electrical signal to maintain the muscle in a tonic state by conversion of muscle fibres to slow-twitch type. This allows long-term tonic contraction of the gracilis muscle to maintain continence. The procedure has an acceptable level of success in around 50% of patients, but at a cost of major surgery and potentially major complications.

Implantable artificial anal sphincters have also been developed and these are placed to encircle the anorectum. Results from the use of the available devices are encouraging but, as with any foreign material, there is a propensity for infection and many have to be removed. Nevertheless, prosthetic devices have a place in the management of a small subset of patients with anal incontinence. Sacral nerve stimulation has been introduced with good effect. This involves insertion of an electrode through the S3 sacral foramina and inducing a low-voltage electrical stimulus. The underlying mechanism is poorly understood but in substantial proportion of selected patients the effects are dramatic. Another surgical option for the patient with anal incontinence is the creation of a permanent colostomy. Although this might be seen as an admission of failure, a well-sited stoma and professional input from a stoma care specialist can transform a patient’s life, from being afraid to leave the house to leading a virtually normal existence.

The management of anal incontinence remains imperfect, but it is clear that patients should be managed by specialist surgeons. This allows a full investigative work-up and tailoring of management for individual patients. In such a setting, the management of anal incontinence can be highly successful. Improvements in obstetric practice are reducing the incidence in sphincter and nerve damage during childbirth. Unfortunately, progress in this area is hampered by the fact that it is many decades after the initial insult before patients present with anal incontinence.

Pruritus ani

The condition can be a minor, short-lived episode but may be an all-consuming obsession for some patients. It is a particular problem at night and some patients may unconsciously scratch the perianal region during sleep, resulting in further trauma and irritation. Pruritus ani is a common complaint and may be a symptom of many anorectal disorders, including haemorrhoids, fistulae, fissures, faecal incontinence, anal carcinoma and rectal prolapse. Dermatological conditions can also be associated with pruritus ani, and these include psoriasis, dermatitis, lichen planus and anal warts; skin infections can also be responsible. Fungal infections should be considered, including candida and tinea, especially in the diabetic patient.

Management

Underlying conditions, such as anal cancer, perianal fistula and haemorrhoids, should be treated and diabetes mellitus excluded. If there is evidence of fungal infection, this should be treated with antifungal creams. In cases where all other contributing disorders have been excluded and the condition is idiopathic, full explanation and support for the patient are essential. The cycle of trauma to the delicate perianal skin, followed by irritation and subsequent scratching, should be explained in detail. Advice on avoidance of scratching and a requirement for willpower is essential. In some cases, it may be necessary for the patient to wear cotton gloves in bed, to avoid nocturnal scratching. The use of perfumed soap and strong antiseptics or lotions should be discouraged. The avoidance of nylon undergarments is important to minimize sweating. Particular attention should be paid to the diet, as certain foods (e.g. spicy foods or alcohol) may be responsible. Explanation should be given of the need to avoid over-zealous cleansing of the perianal region after defaecation. Gentle cleaning with toilet paper, followed by washing with mild soap, may be necessary, but it is important to take care to avoid trauma during drying. A simple barrier cream such as is used for nappy rash may be appropriate in some patients, but generally it is best to avoid relying on creams. Although it may take several months to control, it is possible to improve the symptoms of idiopathic pruritus ani in almost all cases, providing there is the necessary commitment from the patient.

Pilonidal disease

Pilonidal disease is a common perianal disorder with a population incidence of 20–30 per 100 000. It is characterized by chronic inflammation in one or more sinuses in the midline of the natal cleft that contain hair and debris (Fig. 17.16). The superficial part of the midline sinus is lined with squamous epithelium, but the tracts themselves are lined with granulation tissue resulting from chronic infection. Pilonidal disease can also affect the digital clefts in hairdressers but this is not discussed here.

Perianal pilonidal disease is more common in males than females, and affects around 2% of the population between the ages of 15 and 35. However, it is very rare after the age of 40, suggesting that there is an aetiological relationship with age and skin character. The disease is vanishingly rare before puberty, when sex hormones act on hair follicles and sebaceous glands. There is enlargement of a hair follicle, which allows the accumulation of extraneous hairs that are caught in the natal cleft itself. A foreign-body reaction is set up, with the result that there is a chronic discharging sinus that attracts other debris and hairs. A sedentary occupation, particularly where sweating is common, is a predisposing factor. The condition was described in large numbers of American troops in the Vietnam war, owing to the use of Jeeps in the warm climate.

Management

The treatment of pilonidal disease may be conservative or surgical. Conservative management comprises attention to natal cleft hygiene and hair removal by depilatory creams or by careful shaving. Antibiotics have a place in the early stages of abscess formation and may avert the need for incision and drainage of an established abscess. Hair removal from the sinus tract itself on a regular basis allows the sinus to drain and avoids the collection of hair and debris.

Surgical drainage is indicated for established abscess and the incision should avoid the midline to minimize the likelihood of recurrence. Debilitating, chronically discharging sinus tracts also merit surgery and there are a number of surgical options. The tracts can be laid open, the granulations removed with a curette and the resultant defects dressed until they heal from the base. Tracts can also be excised and closed primarily with sutures, although the wound is prone to break down and heal by second intention. Unfortunately, the treatment of pilonidal disease is characterized by frequent recurrence, due partly to inadequate or inappropriate surgery in some cases, but mostly to the fact that the underlying aetiology is still present: namely, the natal cleft and a predisposed skin type. Recurrent disease can be treated using rotation flaps to replace the pitted skin with fresh skin from the buttock. For complex recurrent disease, ablation of the natal cleft using a flap procedure (cleft closure) is highly effective but leaves a fairly large unsightly scar. It is important to advise the patient to keep the natal cleft free of hair by depilation after any successful surgical treatment.