ELIGIENDO EL MEJOR TRATAMIENTO
PARA LA FISURA ANAL
Dr. Stanley Goldberg
INTRODUCTION
Anal fissure is a common disorder, which is highly distressed to the patient
often out of proportion to the physical findings that can be demonstrated.
Fissures can be classified as either acute or chronic and may be either primary
idiopathic or secondary. The vast majority of fissures encountered in clinical
practice are of idiopathic primary origin. Patients usually present to the office
complaining of problems with their “hemorrhoids.” A careful history will in most
cases direct the experienced clinician to the correct diagnosis. Classically the
patient will complain of severe sharp searing pain at the time of defecation often
of a hard constipated stool, which is accompanied by a small amount of bright
red bleeding. The pain can last only a few minutes or for several hours after a
bowel movement. The diagnostic can usually be confirmed by gently separating
the buttocks while inspecting the anal verge for signs of a tear in the epithelium.
Once identified, any attempts at instrumentation of the anus or anorectum
should be deferred until treatment can be initiated with the expectation that the
patient can then be comfortably examined to rule out any associated pathology.
On the other hand, patients with chronic fissures can usually tolerate
examination on the first visit. Secondary causes of fissure-in-ano include
Crohn’s disease, ulcerative colitis, syphilis, tuberculosis, leukemia, malignancy
and other disorders. Fissures off the midline should raise the suspicion of an
underlying disease process.
ETIOLOGY AND PATHOGENESIS
Despite what seems to be a rather common straightforward malady, much is
unknown about the etiology and pathogenesis of this disorder. The common
association of the passage of a hard constipated stool with the onset of
symptoms is presumptive evidence that trauma is the initiating factor, yet many
questions remain poorly understood, such as, why fissures are most commonly
in the midline and why some heal spontaneously while others become chronic.
More recent studies have suggested that ischemia may play a role in the
etiology of fissure and may explain some of the questions that have baffled
clinicians managing this disease.
TRAUMATIC THEORY
The etiology of anal fissure is largely speculative but there is general agreement
that the intiating factor is the passage of a large, hard stool that tears the
anoderm thus resulting in a linear split that is then manifest as a fissure. In other
instances, a fissure can be instigated by the passage of an explosive diarrheal
stool. In both events, trauma to the anal canal is the causative factor.
Constipation has also been incriminated in the perpetuation of an anal fissure
because of repetitive trauma to the injured anoderm. This was supported by
Jensen’s finding that anal fissure disease could be dramatically altered by
increasing fiber intake. Jensen has also demonstrated in a case controlled
study that anal fissure results from an inadequate fiber diet and dietary
management can potentially reduce the incidence of this disease. Previous anal
surgery may also be a contributing factor as the resultant scar is inelastic and
tethered and more prone to traumatic injury and fissure formation.
INTERNAL SPHINCTER ABNORMALITY
Although the initiating factor in fissure development is traumatic, its perpetuation
is due to an abnormality of internal sphincter function. Several investigators
have demonstrated high resting pressure in fissure patients. When a rectoanal
inhibitory reflex is elicited, the pressure rises above the normal resting pressure
following the reflex relaxation. This might explain the spasm and pain that
results after anorectal stimulation induced by a bowel motion. The finding of
ultraslow waves in 80% of fissure patients compared to only 5% of controls
adds further evidence for an internal sphincter abnormality. Schouten and
Blankensteijn have reported that ultraslow waves disappear after adequate
internal sphincterotomy when resting pressures are reduced to a normal level.
ISCHEMIA THEORY
One of the most recent and interesting hypothesis has been the proposal that
the underlying pathophysiology for fissure development is ischemia. Gibbons
and Read have suggested that the elevated resting pressure is a primary event
rather than a consequence of the fissure. Excessive resting pressure, could
potentially reduce vascular perfusion pressure to the anoderm to levels that in
other areas of the body would result in ischemic ulceration. The resultant fissure
would then persist because of the chronic ischemia. Their prevalence in men
and in the young could then be explained on the basis of higher resting
pressure in these groups. The predilection for posterior and anterior midline
location might then be explained by the fact that the blood supply approaches
the anus from a lateral perspective thus achieving less perfusion anteriorly and
posteriorly. Similarly the increased frequency of anterior fissures in females may
reflect a poorer blood supply to the anterior midline anoderm.
Klosterhalfen et al published a study on the topography of the inferior rectal
artery and suggest a causal relationship with chronic primary anal fissure.
Postmortem angiography showed that in 85% of cases of nonselected
autopsies the posterior commissure was the end of the capillary system of the
inferior rectal artery and that anastomosis of the rectal arteries at this posterior
site was rare – hence an anastomotical basis for hypoperfusion in the posterior
midline exists. In 15% of autopsy specimens, the posterior commisure was
adequately vascularized by the inferior rectal artery similar in extent to other
areas of the anal canal. They have also demonstrated that major arterial
vessels that pass vertically through the internal sphincter muscle within the
intermuscular septum are liable to strong contusion during increased sphincter
tone. This results in diminished blood supply which may lead to ischemia.
Schouten et al have demonstrated that the anoderm at the posterior midline is
less perfused in fissure patients and have documented that this is a result of the
elevated anal pressure. By using combined laser Doppler flowmetry and anal
manometry in 31 controls and 15 patients with combined chronic posterior
fissures, they have shown that anodermal blood flow in the fissure group was
significantly lower than at the posterior comissure in control patients.
Futhermore, after internal sphincterotomy, all fissures healed and a significant
drop in resting pressure with concomitant rise in anodermal blood flow was
evident. They conclude that the healing is a result of the improvement in
anodermal blood flow.
TREATMENT
ACUTE FISSURE
The mainstay of treatment of an acute anal fissure is the avoidance of
constipation. The repetitive fissure perpetuating cycle of hard stool, pain and
spasm must be broken in order to allow the fissure to heal. A bulk forming agent
should be initiated and dosage adjusted to maintain a formed but soft stool that
is atraumatic to the anoderm during passage. Warm sitz baths are beneficial in
relieving the spasm associated with a fissure. In a study by Dodi et al
monometric measurements of anal canal pressure were obtained from fissure
patients while the anus was submerged in bath water of varying temperatures
(5,23, and 40 degrees Celsius). They demonstrated that resting anal pressure
was reduced by sitz bath at 40 degress Celsius but not at the other
temperatures. Local application of anesthetic ointment creams provides some
symptomatic relief, but they must be applied directly to the fissure. The use of
suppositories is discouraged as they are painful to insert and once inserted
reside above the puborectalis where they are ineffective for the fissure that is
located in the distal anal canal. With proper and timely administration of medical
treatment, about 50-75% of acute anal fissures can be expected to heal. In a
double blind, placebo controlled study, Jensen et al found that the use of
unprocessed bran (5gm three times daily) resulted in a diminished recurrence
rate. Patients taking 15mg of bran a day had a 16% recurrence while those on
7.5mg had a 60% recurrence and those on placebo had a 68% recurrence at
one year. This data would suggest that those patients who heal with medical
management should be maintained on bulk agents for life. Other conservative
measures such as the use of anal dilators, local injection of long acting
anesthetic agents, and the use of sclerosants such as Sortdecal have been
reported but have not gained widespread usage. Botulinum toxin has been
injected into the anal sphincter to effect a time limited paresis of the sphincter
as treatment of an anal fissure. Isolated reports have suggested that healing
can be achieved. The efficacy and safety of this approach remain to be
determined.
Recently, the use of topical bitroglycerine has been suggested as a new and
potentially effective therapy for acute fissure-in-ano and other disorders. The
premise for its use is based on the evidence that internal sphincter hypertonia is
causative for the pain of anal fissure. Nitric oxide has been recently identified as
a messenger for mediation of the anorectal inhibitory reflex in humans.
Nitroglycerine is a nitric oxide donor – hence its potential role in treatment of
this disorder. Gorfine has recently reported excellent relief of pain in all 15
patients treated with 0.5 percent nitroglycerine paste. Complete healing of the
fissure occurred in ten of the patients within two weeks and with in one month in
two patients. Two patients had persistent anal ulcers but were free of pain.
CHRONIC FISSURE
Several features distinguish a chronic fissure from its acute precursor. The
fissure edges become indurated and undermined, the circular fibers of the
internal sphincter are visible at the depths of the ulcer, a sentinel pile forms as
well as the hypertrophied anal papilla. Once this stage is reached, it is very
unlikely that spontaneous healing will occur and surgical intervention is usually
necessary. The indications, therefore, for surgery are continued pain and
bleeding related to the fissure, which has failed all efforts at conservative
treatment.
CLASSIC EXCISION
Although this technique still has some proponents, it has largely been
abandoned.
VY-ADVANCEMENT FLAP
This procedure still has a place, particularly in patients who have a significant
stenosis related to the chronic fissure.
ANAL DILATION
This technique still remains popular especially in the United Kingdom. The
technique requires forceful disruption of the internal sphincter fibers in a
relatively uncontrolled manner. There is a risk of significant incontinence,
particularly in the older population, and recurrence rates are reported in the
range of 10-30%.
LATERAL INTERNAL SPHINCTEROTOMY
Initial experience with internal sphincterotomy for the surgical treatment of
fissure-in-ano was with the posterior sphincterotomy. However, this was
accompanied by prolonged healing and by a significant incidence of anal
incontinence. Much of this incontinence was felt to be due to a keyhole
deformity that was noticed after posterior sphincterotomy. Eisenhammer
suggested that a lateral placement of the internal sphincter division would
produce less of a trough and would, therefore, be less likely to cause altered
continence. This technique has been widely adopted in the surgical
management of fissure-in-ano. It can be performed using an open technique or
a closed technique as first proposed by Notaras.
A recent review of our experience comparing the open technique to the closed
technique has been completed by Garcia-Aguilar et al. The charts of 864
patients with chronic anal fissure who underwent internal sphincterotomy as a
single procedure over 5 years by our faculty of 12 colorectal surgeons were
reviewed. Open sphincterotomy was performed in 521 patients, while 343 had
closed lateral internal sphincterotomy. There was no difference in sex or age
between the groups. A questionnaire inquiring about clinical outcome, changes
in continence and degree of satisfaction with the procedure was mailed to all
patients. A total of 565 (65.2%) patients, 333 (63.7%) with open sphincterotomy,
and 231 (67.3%) with closed sphincterotomy returned their questionnaires.
Average follow-up was three years. Difference in persistence of symptoms
(3.4% open vs. 5.3% closed), recurrence of the fissure (10.9% open vs. 11.7%
closed), and need for reoperation (3.4% open vs. 4.0% closed) were not
statistically significant. There was, however, a statistically significant difference
in the percentage of patients with impairment in continence between those who
underwent open and those who had a closed internal sphincterotomy.
Incontinence flatus
Soiling underwear
Incontinence stool
Open (%)
30.3
26.7
11.8
Closed (%) p
23.6
0.062
16.1
0.001
3.1
0.001
More patients undergoing closed (64.4%) than open (49.7%) were very satisfied
(Visick I) with the results of the procedure. We conclude that closed internal
sphincterotomy is the procedure of choice in the management of chronic anal
fissure because it is as effective as open sphincterotomy in the management of
symptoms but is associated with less impairment of anal continence and more
patient satisfaction.