Anal fissure is a common anorectal disorder resulting in anal pain and bleeding. Fissures can either heal spontaneously and be classified as acute, or persist for 6 or more weeks and be classified as chronic, ultimately necessitating treatment. Anal stenosis is a challenging problem most commonly resulting from trauma, such as excisional hemorrhoidectomy. This frustrating issue for the patient is equally as challenging to the surgeon. This article reviews these 2 anorectal disorders, covering their etiology, mechanism of disease, diagnosis, and algorithm of management.
Key points
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Anal fissure is arbitrarily classified as acute and chronic fissure, with the cutoff being nonhealing for 6 weeks or more.
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Whereas most acute fissures heal spontaneously, chronic anal fissures require treatment.
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The foundation of treatment relies on reversing internal sphincter hypertonia, thereby improving blood perfusion and promoting healing.
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Treatment options include:
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Nonsurgical: ointments (nitroglycerin, diltiazem, nifedipine)
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Chemodenervation: type A botulinum toxin
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Surgical: lateral internal sphincterotomy
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Algorithm of treatment usually starts with ointments or chemodenervation. Given the possibility of anal continence compromise, surgery is used as a last resort for refractory, nonhealing fissures in patients with hypertonic sphincters.
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Mucosal advancement flaps are a viable surgical option for low-pressure fissures, or those at high risk for postoperative incontinence.
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The most common cause of anal stenosis is overzealous hemorrhoidectomy.
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Anal stenosis is classified based on the level, degree, and area of anal canal involved.
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Management of anal stenosis is challenging, and should be conducted by an experienced surgeon who is familiar with the disease.
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Management is tailored based on etiology and the level, degree, and area involved in stenosis.
Introduction: background, etiology, and pathophysiology
Anatomic and Physiologic Background
The functional anal canal starts at the anorectal ring and extends 3 to 4 cm to the anal verge. Proximally it is lined with columnar cells, which transition to squamous cells approximately 1 to 1.5 cm proximal to the dentate line; hence the term anal transition zone. Distal to the dentate line the multilayered squamous cell lining is rich with somatic nerves. Unlike skin, this area lacks sebaceous and skin glands and hair follicles, and is commonly referred to as the anoderm.
The anal canal lies at an angle with the rectum, owing to the effect of the sling-like puborectalis muscle around the rectum. The internal anal sphincter (IAS) is a thickened continuation of the longitudinal smooth muscle layer of the rectum. At rest the IAS is continuously contracted; is responsible for resting anal pressure, and causes passive continence. On defecation, the puborectalis muscle relaxes, resulting in straightening of the anorectal angle. The IAS relaxes, via the rectoanal inhibitory reflex, and the delicate pliable anoderm stretches and dilates to accommodate the passage of a column of stool.
Physiology of IAS Muscle Contraction
The IAS comprises smooth muscle fibers that are continuously contracted and regulated by the autonomic and enteric nervous systems. Contraction is mediated via an increase in cytoplasmic calcium. Conversely, a decrease in cytoplasmic calcium would result in relaxation.
β-Adrenoceptor stimulation induces the return of cytosolic calcium to the sarcoplasmic reticulum via cyclic adenosine monophosphate, which leads to muscle relaxation. Similarly, relaxation is induced by nonadrenergic, noncholinergic nitric oxide (NO), which is mediated via cyclic guanosine monophosphate (cGMP). Alternatively, blocking direct influx of extracellular calcium through the membranes of calcium channels would achieve the same results; α-adrenoceptor stimulation leads to the release of calcium from the sarcoplasmic reticulum, resulting in contraction.
Epidemiology
Fissure in ano is a longitudinal or elliptical tear in the mucosal lining of the anal canal distal to the dentate line. At this location, the anoderm lining is composed of multiple layers of squamous epithelium and is richly innervated with pain fibers. Anal fissures (AFs) result in significant morbidity and reduction of quality of life in otherwise healthy young individuals.
Although fissures are more commonly encountered in a young age group, with equal ratio among both genders, they can also affect extremes of age. The exact incidence is unknown, likely because many patients with acute fissures do not seek medical advice, and improve without treatment. However, it has been suggested that the lifetime incidence is 11%.
Fissures are usually single, and lie in the posterior midline in 80% to 90% of cases. Anterior midline AFs are most commonly found in women. About 3% to 10% of AFs occur in the postpartum period, and these are often in the anterior midline.
Primary AFs are idiopathic, usually anterior or posterior, and are not caused by underlying disease. Secondary fissures often occur in the lateral positions and are associated with other disease processes. Multiple fissures should raise suspicion of other causes such as inflammatory bowel disease (mainly Crohn disease), human immunodeficiency virus, syphilis, tuberculosis, cancer, or leukemia. Alternatively, fissures refractory to treatment should prompt examination under anesthesia and biopsy to rule out malignancy.
Primary fissures tend to occur more commonly in young age groups of both genders. Those fissures occurring in persons older than 65 years are more likely to be a secondary, so testing to rule out inciting pathology should be performed. AFs are arbitrarily classified as acute AF (AAF) and chronic AF (CAF) based on the duration of the disease process, with the cutoff being 6 weeks of persistent symptoms.
Etiology
Although AF is a commonly encountered anal problem, the exact etiology is poorly defined. The following mechanisms are thought to cause this condition.
Constipation and low-fiber diet
Trauma by passage of hard stool is thought to be an initiating factor. However, it has been reported that constipation occurs in only 1 in 4 patients; furthermore, in about 4% to 7% of instances fissure will follow bouts of diarrhea. Nevertheless, a low-fiber diet seems to be associated with an increased risk of developing a fissure.
Trauma during pregnancy
Up to 10% of chronic AFs occur postpartum, thought to be secondary to shearing forces from the fetus on the anal canal. Alternatively, the anal canal mucosa loses pliability and becomes tethered to underlying tissues, rendering it more susceptible to trauma while stretching during defecation. This type of AF tends not to be associated with high resting anal pressures.
Internal anal sphincter hypertonicity/spasm
As mentioned earlier, mean resting anal pressure (MRAP) is maintained by continuous contraction of the IAS. This contraction is mediated by α-adrenergic pathways as well as inherent myogenic tone. Once thought to be secondary to anal pain, high internal sphincter tonicity is now envisioned as a plausible cause of chronic AF. There has been evidence relating AF to high MRAP secondary to spasm of the IAS. Postmortem angiographic studies demonstrate relatively low perfusion at the posterior commissure of anal canal, where 90% of fissures are found. Doppler laser flowmetric study of the anodermal blood flow confirms the same findings. In healthy volunteers, the resting anal canal pressure is about 80 to 100 mm Hg, almost approaching the intra-arterial systolic pressure of the inferior rectal artery. Hypertonia of the IAS would impede blood flow, creating an area of relative ischemia and resulting in superficial ischemic ulcer (ie, AF). This correlation between abnormally high anal pressure and decreased anal blood flow is the foundation of AF treatment.
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