ANAL DISORDERS

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.

Anal fissure is a split in the lining of the distal anal canal. It is a

common condition and particularly affects young and otherwise
healthy adults, with an equal sex distribution. The classical symptoms are anal pain during and after defecation and fresh bleeding
per rectum. The pain is usually severe and often described as
passing glass, whilst the bleeding is generally modest. Pruritus
ani accompanies anal fissures in 50% of cases.
By firm traction on the buttocks, the fissure may be seen as a
linear split in the lining of the distal anal canal, but there often
is marked anal spasm that obscures the view. The combination
of spasm and pain often precludes a digital rectal or proctoscopic
examination. An acute fissure usually has sharply demarcated
fresh mucosal edges, and there may be granulation tissue in its
base. With increasing chronicity, the margins of the fissure become
indurated, and there is a distinct lack of granulation tissue. Horizontal white fibres of the internal anal sphincter may be evident
in the base of the mucosal defect, and secondary changes (such
as a sentinel skin tag or hypertrophied anal papilla) frequently
accompany chronic fissures.
Most fissures are acute and relatively short-lived, resolving
spontaneously or with simple dietary modification to increase
dietary fibre and stool-softening laxatives when appropriate. The
distinction between acute and chronic fissures is somewhat arbitrary, and cannot be made reliably solely on the appearance of the
fissure. Fissures persisting after 6 weeks despite straightforward
dietary measures usually are designated as chronic. Although a
proportion (probably <10%) of chronic fissures eventually resolve
with conservative measures, most require further intervention to
heal.
Fissures are usually single and most usually in the posterior
midline, but 10% of women and 1% of men have anterior fissures.
Postpartum fissures account for 311% of all chronic fissures and
tend to be anterior. Multiple fissures or those in a lateral position
may be associated with underlying inflammatory bowel diseases,
syphilis or immunosuppression. Fissures that are resistant to treatment should prompt further investigation, including examination
under anaesthesia and appropriate biopsy. This contribution
should be read in conjunction with Acheson/Scholefield, page
165 and Maxwell-Armstrong, page 161.

Local ischaemia: chronic anal fissure has been described as an

ischaemic ulcer. In cadaver studies, angiography of the inferior
rectal arteries (which supply the distal anal canal) has shown a
paucity of arterioles at the posterior commissure, the site for which
fissures have a predilection in 85% of cases. Blood flow to the
distal anal canal, measured by laser Doppler flowmetry, is inversely
proportional to resting anal pressure. Blood vessels traversing the
sphincter en route to the anal mucosa may be compressed, resulting in compromised perfusion of the anal mucosa and fissure. As
the anal spasm appears to predate the fissure, this would support
an ischaemic basis for chronic fissures.
Trauma during childbirth: of patients with chronic fissures, 11%
develop symptoms following childbirth. The risk increases with
traumatic deliveries, and the fissures are commonly anterior.
Shearing forces from the foetal head on the anal mucosa may be
significant. Notably, these patients tend not to display the raised
resting anal canal pressures generally associated with other patients
with chronic fissures.
Differential diagnoses
Haemorrhoids present with fresh rectal bleeding, but are usually painful only when thrombosed.
Fistula in ano may also present with perianal pain, discharge or
bleeding. A perianal cutaneous opening of the fistula may be seen
clearly on examination, but assessment under general anaesthesia
may be required to differentiate between fistula and fissure.
Colorectal cancer blood mixed with the stool should immediately alert the clinician to the possibility of underlying malignancy.
These cancers may also present with fresh bleeding per rectum,
and even anal pain with low anorectal cancers. It is wise to have
a high index of suspicion, particularly in elderly patients, in order
to avoid delayed treatment of malignancy. Where there is doubt
concerning the diagnosis, examination should be performed under
general anaesthesia.

M Jonas-Obichere is a Specialist Registrar on the North-West Thames

General Surgery rotation, London, UK.
John H Scholefield is Professor of Surgery at the University Hospital,
Nottingham, UK.

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ANAL DISORDERS

Treatment
The treatment for anal fissures is summarized in Figure 1.

sphincter led to the widespread use of organic nitrates in the

treatment of chronic anal fissure. Glyceryl trinitrate (GTN) and
isosorbide dinitrate are metabolized at a cellular level to release
NO and have been shown to heal chronic fissures.
The dose of GTN has not been standardized and depends on
the concentration and the volume of ointment applied. A regimen
using a pea-sized amount of 0.2% GTN ointment (approximately
0.5 g), applied 2 or 3 times daily to the distal anal canal for 8
weeks, has been shown to heal two-thirds of chronic fissures.
Headaches are a reversible side-effect experienced by over 50%
of those using GTN: higher-concentration preparations increase
the incidence and severity of the headaches.
The effect of nitrates on the internal sphincter appears to be
reversible. Long-term follow-up of patients treated with GTN has
shown that 27% experience recurrent symptoms within a median
of 2 years, but most (73%) resolve with further GTN.

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

Botulinum toxin: botulinum toxin A (produced by Clostridium

botulinum) is a lethal neurotoxin which binds to presynaptic
cholinergic nerve terminals and inhibits the release of acetylcholine
at the neuromuscular junction. Studies have shown that injection
of botulinum toxin A in a non-lethal dose (e.g. 20 IU) into the anal
sphincter lowers resting anal pressure and heals up to 96% of fissures. The mode of action of botulinum toxin on the internal anal
sphincter is unclear as there are no cholinergic receptors.
The treatment has a prolonged effect, but is ultimately reversible. It is invasive, and complications (e.g. perianal haematoma,
sepsis, pain during injection) have been reported. Despite evidence
to support its efficacy, the role of botulinum toxin in the management of chronic fissures remains unclear.

Surgery: failure of medical therapy in the presence of persistent

symptoms warrants surgical intervention. Anal dilatation is a nonstandardized uncontrolled procedure, which disrupts and may
lead to permanent damage of the sphincter mechanism. Healing
rates of 4070% have been reported with this technique, and
recurrence rates of up to 56%. Of greater concern are reports of
incontinence to flatus and soiling in 39%, and faecal incontinence
in 16%. A meta-analysis has shown that internal sphincterotomy
is superior to anal dilatation in terms of healing, and poses less
of a threat to continence.
A lateral incision is preferable to a posterior midline, as the latter
takes longer to heal and may heal with guttering, which may lead
to imperfect closure of the anal canal or trapping of faeces with
resultant soiling. There was no demonstrable difference between
open versus closed technique for sphincterotomy. Both techniques
are performed through a small lateral incision at the anal margin,
the internal sphincter being incised under direct vision in the
open technique, or blind by the guidance of an examining finger
per anus in the closed technique.
To avoid complications in female patients, and particularly those
with postpartum fissures, it is recommended that the anal sphincter
be assessed using anorectal ultrasound and manometry before surgical intervention. In patients in whom the sphincter is compromised
and resting anal pressure is not elevated, an anal advancement flap
may be more appropriate rather than jeopardize anal continence
through further iatrogenic injury to the sphincter.

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Pruritus ani

Management of pruritus ani

Pruritus ani is a symptom, not a diagnosis. Characterized by

intense perianal itching or burning, it is common: affecting 5%
of population over 40 years of age, with a male preponderance of
4:1. The onset is insidious, but symptoms may become intractable.
Scratching produces short-lived symptomatic relief and damages
the skin. The cycle of itching and scratching becomes self-propagating, and eventually leads to lichenification of the perianal skin
which appears white with fine fissures. Symptoms are usually
worse at night, and in the summer, when sweating is greatest.

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

present, are always associated with pruritus ani.

Sexually transmitted diseases can lead to pruritus ani, particularly with anal coition.
Scabies infection usually presents with more generalized itching
but, like pediculosis pubis, may cause pruritus ani.
Pinworms (Enterobius vermicularis) are a common cause in
children, and in adults who live with children. Threadworms are
a cause in adults and may appear as thin white threads around
the anus.
Drugs steroids and immunosuppressants may cause pruritus
ani. Antibiotics (especially oral tetracyclines) or prolonged administration of metronidazole (possibly by suppressing the normal
gut flora) are also associated with pruritus ani. Quinidine and
colchicine, may cause faecal leakage, precipitating pruritus ani.
Pyschogenic factors in idiopathic pruritus, a psychological
aetiology is often inferred. However, objective personality testing
has not revealed significant differences in the profiles of patients
with idiopathic versus secondary pruritus ani.

Management of idiopathic pruritus ani

Simple hygienic measures
Wash with water twice daily and after defecation
Avoid perfumed soaps or antiseptics
Pat dry or blow dry (with hairdryer)
Avoid scratching
Cotton gloves at night (to avoid trauma from scratching during
sleep)
Avoid creams/ointments unless prescribed
Cotton underwear (to reduce sweating)
Loose fitting underwear and trousers
Cotton pledget just inside anus to absorb moisture

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.
u

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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