11/1/2017 Anorectal Abscess: Background, Anatomy, Pathophysiology

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Anorectal Abscess
Updated: Dec 27, 2016
Author: Andre Hebra, MD; Chief Editor: John Geibel, MD, DSc, MSc, AGAF more...

OVERVIEW

Background
An anorectal abscess originates from an infection arising in the cryptoglandular epithelium lining the
anal canal. The internal anal sphincter is believed to serve normally as a barrier to infection passing
from the gut lumen to the deep perirectal tissues. This barrier can be breached through the crypts of
Morgagni, which can penetrate through the internal sphincter into the intersphincteric space.

Once infection gains access to the intersphincteric space, it has easy access to the adjacent perirectal
spaces. Extension of the infection can involve the intersphincteric space, ischiorectal space, or even
the supralevator space. In some instances, the abscess remains contained within the intersphincteric
space. The severity and depth of the abscess are quite variable, and the abscess cavity is often
associated with formation of a fistulous tract. For that reason, fistulas are also discussed in this article
where relevant.

The variety of anatomic sequelae of the primary infection is translated into variable clinical
presentations. The relatively simple perianal abscess is to be distinguished from the more complex
perirectal abscesses. Treatment also differs according to the type of abscess present.

For patient education resources, see the Esophagus, Stomach, and Intestine Center and the Digestive
Disorders Center, as well as Anal Abscess, Rectal Pain, and Rectal Bleeding.

Anatomy
Normal anatomy demonstrates anywhere from 4-10 anal glands lying at the level of the dentate line,
which divides the squamous epithelium distally and the columnar epithelium proximally. Obstruction of
these anal glands by debris leads to stasis, bacterial overgrowth, and abscess formation that extends
into the intersphincteric groove between the internal and external anal sphincters. [1] From this space,
the abscess can spread along various potential spaces.

Anorectal abscesses are classified according to their anatomic location; the following are the most
common locations (see the image below):

Perianal
Ischiorectal
Intersphincteric
Supralevator

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11/1/2017 Anorectal Abscess: Background, Anatomy, Pathophysiology

Illustration of major types of anorectal abscesses (submucosal type not pictured).

View Media Gallery

Perianal abscesses represent the most common type of anorectal abscesses, accounting for
approximately 60% of reported cases. [1, 2, 3, 4] These superficial collections of purulent material are
located beneath the skin of the anal canal and do not transverse the external sphincter.

Ischiorectal abscesses are the next most common type. These abscesses form when suppuration
transverses the external anal sphincter into the ischiorectal space. An ischiorectal abscess may
traverse the deep postanal space into the contralateral side, forming a so-called horseshoe abscess.

Intersphincteric abscesses, the third most common type, result from suppuration contained between
the internal and external anal sphincters. They may lie completely within the anal canal, leading to
severe pain, and may only be found by digital rectal examination or anoscopy.

Supralevator abscesses, the least common of the four major types, may form from cephalad extension
of the intersphincteric abscess above the levator ani or from caudal extension of a suppurative
abdominal process (eg, appendicitis, diverticular disease, gynecologic sepsis) into the supralevator
space. These abscesses may be diagnosed by means of computed tomography (CT), and they cause
pelvic and rectal pain.

According to the widely used Parks classification system, anorectal fistulas may also be classified into
four major types, as follows [5] :

Intersphincteric (70%) - Found between the internal and external sphincters

Transsphincteric (23%) - Extends through the external sphincter into the ischiorectal fossa
Extrasphincteric (5%) - Passes from the rectum to the skin through the levator ani
Suprasphincteric (2%) - Extends from the intersphincteric plane through the puborectalis, exiting
the skin after traversing the levator ani

The characteristics of perianal fistulas vary according to their anatomic location. According to the
Goodsall rule, the external opening of a fistulous tract located anterior to a transverse line drawn
across the anal verge is associated with a straight radial tract of the fistula into the anal canal/rectum,
whereas an external opening posterior to the transverse line follows a curved, fistulous tract to the
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11/1/2017 Anorectal Abscess: Background, Anatomy, Pathophysiology

posterior midline of the rectal lumen (see the image below). This rule is important for planning surgical
treatment of the fistula (see Treatment).

Goodsall rule for anorectal fistulas. Fistulas that exit in posterior half of rectum generally follow curved course
toward posterior midline, whereas those that exit in anterior half of rectum usually follow radial course to dentate
line.
View Media Gallery

Pathophysiology
Perirectal abscesses and fistulas represent anorectal disorders arising predominantly (~90% of cases)
from the obstruction of anal crypts, [4] possibly involving increased sphincter tone. [6] Infection of the
now static glandular secretions results in suppuration and abscess formation within the anal gland.
Typically, the abscess forms initially in the intersphincteric space and then spreads along adjacent
potential spaces.

Etiology
Both aerobic and anaerobic bacteria have been found to be responsible for abscess formation. The
anaerobes most commonly implicated are Bacteroides fragilis, Peptostreptococcus, Prevotella,
Fusobacterium, Porphyromonas, and Clostridium. The aerobes most commonly implicated are
Staphylococcus aureus, Streptococcus, and Escherichia coli. [7] More recent studies have noted
community-acquired methicillin-resistant S aureus (MRSA) as a pathogen leading to abscess
formation. [8, 9]

Approximately 10% of anorectal abscesses may be caused by reasons other than anal gland
infection, including Crohn disease, trauma, immunodeficiency resulting from HIV infection or
malignancy (both hematologic and anorectal cancer), tuberculosis, hidradenitis suppurativa, sexually
transmitted diseases, radiation therapy, foreign bodies, perforated diverticular disease, inflammatory
bowel disease, or appendicitis (a rare cause of supralevator abscesses). [1]

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11/1/2017 Anorectal Abscess: Background, Anatomy, Pathophysiology

Epidemiology
United States and international statistics
Approximately 30% of patients with anorectal abscesses report a previous history of similar abscesses
that either resolved spontaneously or required surgical intervention.

The incidence of abscess formation appears to be higher in spring and summer. Whereas
demographics point to a clear disparity in the occurrence of anal abscesses with respect to age and
sex, no obvious pattern exists among various countries or regions of the world. Although it has been
suggested that there is a direct relation between the formation of anorectal abscesses and bowel
habits, frequent diarrhea, and poor personal hygiene, this relation remains unproven.

Age- and sex-related demographics

The peak incidence of anorectal abscesses is in the third and fourth decades of life. [10] These
abscesses are also quite common in infants (see Anorectal Abscesses in Children). The exact
mechanism is poorly understood but does not appear to be related to constipation. Fortunately, this
condition is quite benign in infants, rarely necessitating any operative intervention other than simple
drainage. [11]

Men are affected more frequently than women are, with a male-to-female predominance of 2:1 to 3:1.
[10]

Prognosis
Overall mortality from anorectal abscesses is quite low. [2]

Early data indicated that abscess formation recurred in approximately 10% of patients, with chronic
fistula-in-ano occurring in as many 50% of patients. [1, 2, 12] A later study found that 37% of patients
developed chronic anal fistula or recurrent sepsis. [6] In this study, risk factors were age younger than
40 years and nondiabetic status; no difference in these complications was noted with regard to HIV
status, sex, antibiotic usage, or smoking status.

Approximately two thirds of patients with rectal abscesses who are treated by incision and drainage or
by spontaneous drainage will develop a chronic anal fistula. After fistula formation, multiple
complications may develop after surgery. As many as 43% of patients may experience fecal
incontinence after surgical repair for complex fistula-in-ano. [13] Other postoperative complications
include temporary postejaculation urethral irritation and postoperative urinary retention. [14]
Constipation may also occur as a result of pain on defecation.

The recurrence rate of anorectal fistulas after fistulotomy, fistulectomy, or the use of a seton is about
1.5%. The success rate of primary surgical treatment with fistulotomy appears to be fairly good. [15]

Clinical Presentation

References

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Media Gallery

Illustration of major types of anorectal abscesses (submucosal type not pictured).

Goodsall rule for anorectal fistulas. Fistulas that exit in posterior half of rectum generally follow
curved course toward posterior midline, whereas those that exit in anterior half of rectum usually
follow radial course to dentate line.
Goodsall rule for anorectal fistulas. Note curved nature of posterior fistulas and radial (straight)
orientation of anterior fistulas.

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Contributor Information and Disclosures

Author

Andre Hebra, MD Chief, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, Medical
University of South Carolina College of Medicine; Surgeon-in-Chief, Medical University of South
Carolina Children's Hospital

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, Florida Medical
Association, Society of American Gastrointestinal and Endoscopic Surgeons, Children's Oncology
Group, International Pediatric Endosurgery Group, American Academy of Pediatrics, American
College of Surgeons, American Medical Association, American Pediatric Surgical Association, Society
of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical
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Congress, Southern Medical Association

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, AGAF Vice Chair and Professor, Department of Surgery, Section of
Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale
University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New
Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, AGAF is a member of the following medical societies: American
Gastroenterological Association, American Physiological Society, American Society of Nephrology,
Association for Academic Surgery, International Society of Nephrology, New York Academy of
Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Acknowledgements

Marc D Basson, MD, PhD, MBA, FACS Professor, Chair, Department of Surgery, Assistant Dean for
Faculty Development in Research, Michigan State University College of Human Medicine

Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega
Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa,
and Sigma Xi

Disclosure: Nothing to disclose.

Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio
Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American
College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National
Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of
Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of
Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of
Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Nizar Kifaieh, MD, FACEP Assistant Professor, Medical Director, Department Of Emergency
Medicine, State University of New York Downstate Medical Center

Nizar Kifaieh, MD, FACEP is a member of the following medical societies: American Academy of
Emergency Medicine, American College of Emergency Physicians, American College of Physician
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Executives, American Medical Association, New York County Medical Society, and Society for
Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical
Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Patrick B Thomas, MD Fellow, Department of Pediatric Surgery, Texas Children's Hospital

Disclosure: Nothing to disclose.

Walter W Valesky Jr, MD Clinical Assistant Instructor, Department of Emergency Medicine, Kings
County Hospital, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

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