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Pathogenesis
The pathogenesis of anal fissure is poorly understood. Surgical
dogma states that a hard stool traumatizes the anal mucosa.
However, only 1 in 4 patients reports constipation and symptoms
follow diarrhoea in 47% of cases.
Anal Fissure
M Jonas-Obichere
John H Scholefield
Internal anal sphincter hypertonia: patients with chronic fissures generally have hypertonicity of the internal anal sphincter
and raised resting anal pressures (see Farouk, page 184a), but the
causative mechanisms are unclear. The normal range is 5080
cmH2O. The administration of pharmacological agents (e.g. organic
nitrates, calcium channel blockers, botulinum toxin) that relax the
internal anal sphincter, (effectively reducing anal canal pressure)
can lead to healing in most chronic fissures. This effect on the
muscle is reversible, however, and resting anal pressures return
to pre-treatment values after a fissure has healed.
These findings suggest that the internal sphincter hypertonia
and consequent anal spasm may predate the onset of the fissure.
Furthermore, anal spasm probably is not a response to pain,
because the application of topical local anaesthetic to a fissure
alleviates the discomfort but does not reduce the anal spasm.
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ANAL DISORDERS
Treatment
The treatment for anal fissures is summarized in Figure 1.
Acute fissure: over 90% of anal fissures are of short duration and
heal spontaneously or with simple measures.
Chronic fissure: treatment is directed at lowering resting anal
pressure. Traditionally, this was achieved surgically by manual
anal dilatation or internal sphincterotomy, but both procedures
carry a risk of impaired anal continence. More recently, various
pharmacological agents (see below) have been shown to lower
anal pressure and heal fissures. This so-called chemical sphincterotomy has become accepted first-line treatment for chronic
fissures in many centres.
Calcium channel blockers diltiazem and nifedipine are prescribed widely in clinical practice as antianginal and antihypertensive agents. They act by blocking slow L-type calcium channels
in vascular smooth muscle, and recently have also been shown to
lower resting anal pressure presumably by a similar action on the
internal anal sphincter smooth muscle. Topical diltiazem (2 cm of
2% gel squeezed from the tube, or approximately 0.7 g) has been
shown to heal 6575% of chronic fissures. Oral nifedipine, 20 mg
orally twice daily, has also been shown to heal 9 of 15 chronic
fissures, and topical nifedipine may also be beneficial.
Organic nitrates the recognition of nitric oxide (NO) as
a neurotransmitter mediating relaxation of the internal anal
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ANAL DISORDERS
Pruritus ani
Pruritus ani
Aetiology
Pruritus ani may be idiopathic, or secondary to an underlying
cause. Traditionally it was believed that most cases were idiopathic,
but recent studies put the incidence of idiopathic pruritus ani at
525%. The management of idiopathic pruritus ani is detailed
in Figure 2.
Systemic disease diabetes mellitus is the most common:
hyperglycaemia predisposes to cutaneous candidiasis. Lymphoma,
vitamin A and D deficiencies and pellagra are other causes.
Mechanical factors excessive cleaning of the perineum, the
use of strong soaps, deodorants and perfumed wipes traumatize
the skin or cause sensitization. Conditions such as hyperhydrosis,
chronic diarrhoea or anal incontinence lead to excessive moisture
and irritation of the perianal area by faecal matter. Haemorrhoids,
anal fissure, fistula in ano and rectal prolapse may cause anal
discharge, which acts as an irritant to the perianal skin.
Dermatological conditions psoriasis is the most common; seborrhoeic and contact dermatitis are other causes. Pruritus ani may
be the presentation of premalignant conditions such as Bowens
disease, or a manifestation of extramammary Pagets disease.
Infections reddened perianal skin with a clearly demarcated
edge is suggestive of fungal infection, a common cause of pruritus
ani. Candida albicans is often present in anal skin scrapings, but
is not usually the cause of pruritus ani, except in diabetic patients
(where hyperglycaemia predisposes to cutaneous candidiasis). Dermatophyte infections, however, are found less often but, when
Management
The management of pruritus ani is outlined in Figure 3.
Investigation of the colon is advisable where there are any relevant bowel symptoms, and particularly in patients aged over 50
years. Appropriate treatment of underlying anal pathology usually
leads to resolution of symptoms. Any pruritic lesion that persists
after adequate treatment should be biopsied.
Dermatological causes general dermatological conditions
can cause localized perianal reactions, and there may be clues
elsewhere on the body. Patients with longstanding pruritus ani in
the absence of colorectal pathology should be referred to a dermatologist for patch testing as many have developed sensitization
to topical preparations.
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Miscellaneous
Calamine lotion and carbolic lotion are effective, but not widely
available
An antihistamine at bedtime, acting both as an antipruritic and
sedative, may be helpful
2
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