The external sphincter forms the bulk of the anal sphincter complex and, although traditionally it has been subdivided into deep, superficial and subcutaneous portions, it is a single muscle which is variably divided by lateral extensions from the longitudinal muscle layer.
The internal sphincter
The internal sphincter is the thickened (2–5 mm) distal continuation of the circular muscle coat of the rectum, which has developed special properties and which is in a tonic state of contraction. This involuntary muscle commences where the rectum passes through the pelvic diaphragm and ends above the anal orifice.
The intersphincteric plane
Between the external sphincter muscle laterally and the longitudinal muscle medially exists a potential space, the intersphincteric plane. This plane is important as it contains intersphincteric anal glands and is also a route for the spread of pus.
The epithelium and subepithelial structures
The pink columnar epithelium lining the rectum extends through the anorectal ring into the surgical anal canal. Just below the level of the anal valves there is an abrupt, albeit wavy, transition to stratified squamous epithelium, which is the colour of parchment.
Blood supply to the anal canal is via superior, middle and inferior rectal vessels
Lymphatic drainage of the lower half of the anal canal goes to inguinal lymph nodes CONGENITAL ABNORMALITIES
Imperforate anus Imperforate anus strictly, it should be anal ‘agenesis’ or ‘atresia’) has historically been divided into two main groups – high and low – depending on the level of termination of the rectum in relation to the pelvic floor.
Post-anal dermoid The space in front of the lower part of the sacrum and coccyx may be occupied by a soft, cystic swelling – a post-anal dermoid cyst. Hidden in the hollow of the sacrum, it is unlikely to be discovered unless a sinus communicating with the exterior is present or it develops as a result of inflammation.
Differential diagnosis Especially in a child, an anterior sacral meningocoele must be excluded. This enlarges when the child cries and is frequently associated with paralysis of the lower limbs and incontinence. When a discharging sinus is present, a post-anal dermoid will probably be mistaken for a pilonidal sinus or even an anal fistula. Pressure over the sacrococcygeal region with a finger in the rectum may cause a flow of sebaceous material.
Treatment Treatment involves complete excision of the cyst and, if present, the sinus. Pilonidal sinus The term ‘pilonidal sinus’ describes a condition found in the natal cleft overlying the coccyx, consisting of one or more, usually non-infected, midline openings, which communicate with a fibrous track lined by granulation tissue and containing hair lying loosely within the lumen.
Aetiology and pathology
Although acquired theories of development are better accepted than the more historical congenital theories, exact mechanisms of development are speculative. Evidence that supports the acquired theory of origin of pilonidal sinuses can be summarized as follows: • Interdigital pilonidal sinus is an occupational disease of Hairdressers • The age incidence of the appearance of pilonidal sinus (82 per cent occur between the ages of 20 and 29 years) is at variance with the age of onset of congenital lesions. • Hair follicles have almost never been demonstrated in the walls of the sinus. • The hairs projecting from the sinus are dead hairs
•The disease mostly affects men, in particular hairy men.
• Recurrence is common, even though adequate excision of the track is carried out. It is thought that the combination of buttock friction and shearing forces in that area allows shed hair or broken hairs which have collected there to drill through the midline skin.
Clinical features The condition is seen much more frequently in men than in women, usually after puberty and before the fourth decade of life, and is characteristically seen in dark-haired individuals rather than those with softer blond hair (Oldham). Patients complain of intermittent pain, swelling and discharge at the base of the spine, but little in the way of constitutional symptoms. Conservative treatment As the natural history of the condition is usually one of regression, in those whose symptoms are relatively minor, simple cleaning out of the tracks and removal of all hair, with regular shaving of the area and strict hygiene, may be recommended.
Treatment of an acute exacerbation (abscess)
If rest, baths, local antiseptic dressings and the administration of a broad- spectrum antibiotic fail to bring about resolution, the abscess should be drained through a small longitudinal incision made over the abscess and off the midline.
Surgical treatment of chronic pilonidal disease
The multitude of surgical procedures advocated to eradicate pilonidal disease.
ANAL FISSURE
Definition An anal fissure (synonym: fissure-in-ano) is a longitudinal split in the anoderm of the distal anal canal which extends from the anal verge proximally towards, but not beyond, the dentate line.
Aetiology
Classically, acute anal fissures arise from the trauma caused by the strained evacuation of a hard stool or, less commonly, from the repeated passage of diarrhoea.
Clinical features Simple epithelial splits, because of their location involving the exquisitely sensitive anoderm, acute anal fissures are characterized by severe anal pain associated with defaecation. This usually resolves spontaneously after a variable time only to recur at the next evacuation, as well as the passage of fresh blood, normally noticed on the tissue after wiping. Chronic fissures are characterised by a hypertrophied anal papilla internally and a sentinel tag externally (both consequent upon attempts at healing and breakdown).
Causes of secondary fissures:
Crohn’s disease, tuberculosis, sexually transmitted or human
Treatment After confirmation of the diagnosis in the clinic or under anaesthesia, with exclusion of secondary causes of anal ulceration, conservative management should result in the healing of almost all acute and the majority of chronic fissures. Emphasis must be placed on normalisation of bowel habits such that the passage of stool is less traumatic. The addition of fibre to the diet to bulk up the stool, stool softeners and adequate water intake are simple and helpful measures. Warm baths and topical local anaesthetic agents relieve pain.
Operative measures
Lateral anal sphincterotomy
In this operation, the internal sphincter is divided away from the fissure itself – usually either in the right or the left lateral positions. Anal advancement flap HAEMORRHOIDS
Internal haemorrhoids are symptomatic anal cushions and characteristically
lie in the 3, 7 and 11 o’clock positions (with the patient in the lithotomy position). In addition, haemorrhoids may be observed between the main pile masses, in which case they are internal haemorrhoids at the secondary position. External haemorrhoids relate to venous channels of the inferior haemorrhoidal plexus deep in the skin surrounding the anal verge and are not true haemorrhoids. External haemorrhoids associated with internal haemorrhoids (‘interoexternal piles’) result from progression of the latter to involve both haemorrhoidal plexuses and are best thought of as being external extensions of internal haemorrhoids.
Secondary internal haemorrhoids arise as a result of a specific condition, The
most important cause, albeit relatively uncommon, is carcinoma of the anorectum but there are many other causes, which may be categorized as follows: • local, e.g. anorectal deformity, hypotonic anal sphincter; • abdominal, e.g. ascites; • pelvic, e.g. gravid uterus, uterine neoplasm (fibroid, carcinoma of the uterus or cervix), ovarian neoplasm, bladder carcinoma; • neurological, e.g. paraplegia, multiple sclerosis.
Primary internal haemorrhoids
Theories of development
Portal hypertension and varicose veins
Man’s upright posture , lack of valves in the portal venous system and raised abdominal pressure were thought to contribute to the development of anal varicosities. Other vascular causes Historically, some considered haemorrhoids to be haemangiomatous.
Infection Repeated infection of the anal lining, secondary to trauma at defaecation, has been postulated as a cause of weakening and erosion of the walls of the veins of the submucosa. Diet and stool consistency
A fibre-deficient diet results in a prolonged gut transit time, which is
associated with the passage of smaller, harder stools that require more straining to expel.
Anal hypertonia The association between raised anal canal resting pressure and haemorrhoids is well known, but whether anal hypertonia causes symptoms attributable to haemorrhoids or whether anal cushion hypertrophy causes anal hypertonia is a subject of debate. Ageing In contrast to the anal cushion of early life, with age, the supporting structures show a higher proportion of collagen than muscle fibres and are fragmented and disorganised. Current view Shearing forces acting on the anus (for a variety of reasons) lead to caudal displacement of the anal cushions and mucosal trauma.
Clinical features Bleeding, as the name haemorrhoid implies, is the principal and earliest symptom. The nature of the bleeding is characteristically separate from the motion and is seen either on the paper on wiping or as a fresh splash in the pan. Very rarely, the bleeding may be sufficient to cause anaemia. Pain is not commonly associated with the bleeding.
Classification Piles associated with bleeding alone are called first-degree haemorrhoids. Patients may complain of true ‘piles’, lumps that appear at the anal orifice during defaecation and which return spontaneously afterwards (second- degree haemorrhoids), piles that have to be replaced manually (third-degree haemorrhoids) or piles that lie permanently outside (fourth-degree haemorrhoids).
Complications of haemorrhoids _ Strangulation and thrombosis _ Ulceration _ Gangrene _ Portal pyaemia _ Fibrosis
Treatment of complications • Strangulation, thrombosis and gangrene. In these cases, it was formerly believed that surgery would promote portal pyaemia. However, if adequate antibiotic cover is given from the start, this is not found to be so, and immediate surgery can be justified in many patients. Besides adequate pain relief, bed rest with frequent hot baths and warm or cold saline compresses with firm pressure usually cause the pile mass to shrink considerably in 3–4 days.
• Severe haemorrhage. The cause usually lies in a bleeding diathesis or the use of anticoagulants. If such causes are excluded, a local compress containing adrenaline solution, with an injection of morphine and blood transfusion if necessary, will usually suffice. However, after adequate blood replacement, ligation and excision of the piles may be required. Management Exclusion of other causes of rectal bleeding, especially colorectal malignancy, is the first priority. Various proprietary creams can be inserted into the rectum from a collapsible tube fitted with a nozzle, at night and before defaecation. Suppositories are also useful. In those with first- or second-degree piles whose symptoms are not improved by conservative measures, injection sclerotherapy , the submucosal injection of 5 per cent phenol in arachis oil or almond oil, may be advised. For more bulky piles, banding has been shown to be efficacious, but it is associated with more discomfort. The Barron’s bander is a commonly available device used to slip tight elastic bands onto the base of the pedicle of each haemorrhoid.
Operation Indications The indications for haemorrhoidectomy include: • third- and fourth-degree haemorrhoids; • second-degree haemorrhoids that have not been cured by non-operative treatments; • fibrosed haemorrhoids; • interoexternal haemorrhoids when the external haemorrhoid is well defined.
Postoperative complications
Postoperative complications may be early or late.
Early complications include pain, which may require opiate analgesia; retention of urine, especially in men, which rarely may need relief by catheterisation; and reactionary haemorrhage, which is much more common than secondary haemorrhage. Late postoperative complications include: • Secondary haemorrhage. This is uncommon, occurring about the 7th or 8th day after operation. It is usually controlled by morphine but, if the haemorrhage is severe, an anaesthetic should be given and the bleeding controlled. • Anal stricture, which must be prevented at all costs. A rectal examination at the postoperative review will indicate whether stricturing is to be expected. It may then be necessary to give a general anaesthetic and dilate the anus. After that, daily use of the dilator should give a satisfactory result. • Anal fissures and submucous abscesses.
• Incontinence, especially if there has been inadvertent damage to the
underlying internal sphincter.
External haemorrhoids A thrombosed external haemorrhoid relates anatomically to the veins of the superficial or external haemorrhoidal plexus and is commonly termed a ‘perianal haematoma’. It presents as a sudden onset, olive-shaped, painful blue subcutaneous swelling at the anal margin and is usually consequent upon straining at stool, coughing or lifting a heavy weight. The thrombosis is usually situated in a lateral region of the anal margin. If the patient presents within the first 48 hours, the clot may be evacuated under local anaesthesia.
ANORECTAL ABSCESSES
The cryptoglandular theory of intersphincteric anal gland infection (Parks) holds
that, upon infection of a gland, pus, which travels along the path of least resistance, may spread caudally to present as a perianal abscess. Underlying rectal disease, such as neoplasm and particularly Crohn’s disease, may be the cause. Patients with generalised disorders, such as diabetes and acquired immunodeficiency syndrome (AIDS), may present with an anorectal abscess.
Usually produces a painful, throbbing swelling in the anal region. The patient often has swinging pyrexia.
Differential diagnosis
The only conditions with which an anorectal abscess is likely to be confused are abscesses connected with a pilonidal sinus, Bartholin’s gland or Cowper’s gland.
Management
Management of acute anorectal sepsis is primarily surgical, including careful
examination under anaesthesia, sigmoidoscopy and proctoscopy, and adequate drainage of the pus. Pus is sent for microbiological culture and tissue from the wall is sent for histological appraisal to exclude specific causes. Antibiotics are prescribed if there is surrounding cellulitis and especially in those less resistant to infection, such as diabetics. If the pus subsequently cultures skin-type organisms, there will be no underlying fistula and the patient can be reassured. If gut flora are cultured, it is likely, but not inevitable, that there is an underlying fistula. FISTULA-IN-ANO
A fistula-in-ano, or anal fistula, is a chronic abnormal communication, usually
lined to some degree by granulation tissue, which runs outwards from the anorectal lumen (the internal opening) to an external opening on the skin of the perineum or buttock (or rarely, in women, to the vagina).
Anal fistulae may be found in association with specific conditions, such as Crohn’s disease, tuberculosis, lymphogranuloma venereum, actinomycosis, rectal duplication, foreign body and malignancy (which may also very rarely arise within a longstanding fistula), and suspicion of these should be aroused if clinical findings are unusual. However, the majority are termed non-specific, idiopathic or cryptoglandular type.
Presentation
Patients usually complain of intermittent purulent discharge (which may be
bloody) and pain (which increases until temporary relief occurs when the pus discharges). There is often, a previous episode of acute anorectal sepsis that settled (incompletely) spontaneously or with antibiotics, or which was surgically drained. The passage of flatus or faeces through the external opening is suggestive of a rectal rather than an anal internal opening.
Classification
The most widespread and useful classification of anal fistulae is that proposed by Parks, (the internal opening is usually at the dentate line), which results in a primary track whose relation to the external sphincter defines the type of fistula.
Intersphincteric fistulae (45 per cent) do not cross the external sphincter most commonly they run directly from the internal to the external openings across the distal internal sphincter. Trans-sphincteric fistulae (40 per cent) have a primary track that crosses both internal and external sphincters .The primary track may have secondary tracks arising from it, which often reach the roof of the ischiorectal fossa, which may rarely pass through the levators to reach the pelvis and which may spread circumferentially (horseshoe). Suprasphincteric fistulae are very rare, are thought by some to be iatrogenic. Extrasphincteric fistulae run without specific relation to the sphincters and usually result from pelvic disease or trauma.
Clinical assessment
A full medical (including obstetric, gastrointestinal, anal surgical and continence)
history and proctosigmoidoscopy are necessary to gain information about sphincter strength and to exclude associated conditions. The key points to determine are the site of the internal opening; the site of the external opening(s); the course of the primary track; the presence of secondary extensions.
Full examination under anaesthesia should be repeated before surgical
intervention. Dilute hydrogen peroxide, instilled via the external opening, is a very useful way of demonstrating the site of the internal opening; gentle use of probes.
Clinical examination will give some indication of functional anal sphincter length, resting tone and voluntary squeeze; these may be more objectively assessed by manometry, whereas endoanal ultrasound gives useful information about sphincter integrity. Magnetic resonance imaging (MRI) is acknowledged to be the ‘gold standard’ for fistula imaging. Fistulography and computed tomography (CT) both have limitations but are useful techniques if an extrasphincteric fistula is suspected.
Surgical management
Fistulotomy: That the fistulous track must be laid open from its termination to its source.
Fistulectomy
Setons:
Advancement flaps
ANAL INTRAEPITHELIAL NEOPLASIA
Anal intraepithelial neoplasia is a multifocal virally induced dysplasia of the perianal or intra-anal epidermis which is associated with the human papilloma virus. At-risk groups include patients with HIV, as well as immunocompromised patients, women with a history of other genital intraepithelial neoplasia (VIN and CIN) and patients with extensive anogenital condylomata.
It is classified according to the degree of dysplasia on biopsy into AIN I, AIN II
and AIN III, according to the lack of keratocyte maturation and extension of the proliferative zone from the lower third (AIN I) to the full thickness of the epithelium (AIN III).
Presentation
Around 10 per cent of AIN lesions are diagnosed by the pathologist after excision of abnormal skin lesions. Ulceration would suggest progression to invasive anal carcinoma. Patients’ symptoms include pruritis, pain, bleeding and discharge.
Treatment Focal disease may be excised and local excision is effective for lesions <30 per cent of the circumference of the anus. More widespread disease can be dealt with surgically by wide local excision and closure of the resultant defect by flap or skin graft, with or without covering colostomy.
NON-MALIGNANT STRICTURES – ANAL STENOSIS
1. Spasmodic : anal fissure causes spasm of the internal sphincter.
anal squamous cell carcinoma (SCC) is rising, with a direct association with HPV infection, AIN and immunosuppression. Anal SCC is associated with HPV (especially subtypes 16, 18, 31 or 33) in 70–90 per cent of cases .
Pain and bleeding are the most common symptoms,while mass, pruritus or discharge is less common. Advanced tumours may cause faecal incontinence by invasion of the sphincters.
Nowadays, primary treatment is by chemoradiotherapy, small marginal tumours are
still best treated by local excision; radical surgery is indicated in those with persistent or recurrent disease.
(50 Studies Every Doctor Should Know (Series) ) David Y. Hwang, David M. Greer, Michael E. Hochman-50 Studies Every Neurologist Should Know-Oxford University Press (2016)
(50 Studies Every Doctor Should Know (Series) ) David Y. Hwang, David M. Greer, Michael E. Hochman-50 Studies Every Neurologist Should Know-Oxford University Press (2016)
