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Hemorrhoids
Updated: Jan 18, 2017
Author: Scott C Thornton, MD; Chief Editor: John Geibel, MD, DSc, MSc, AGAF more...
OVERVIEW
Background
Hemorrhoids are swollen blood vessels in the lower rectum. They are among the most common
causes of anal pathology, and subsequently are blamed for virtually any anorectal complaint by
patients and medical professionals alike. Confusion often arises because the term "hemorrhoid" has
been used to refer to both normal anatomic structures and pathologic structures. In the context of this
article, "hemorrhoids" refers to the pathologic presentation of hemorrhoidal venous cushions.
Hemorrhoidal venous cushions are normal structures of the anorectum and are universally present
unless a previous intervention has taken place. Because of their rich vascular supply, highly sensitive
location, and tendency to engorge and prolapse, hemorrhoidal venous cushions are common causes
of anal pathology. [1] Symptoms can range from mildly bothersome, such as pruritus, to quite
concerning, such as rectal bleeding.
Although hemorrhoids are a common condition diagnosed in clinical practice, many patients are too
embarrassed to ever seek treatment. Consequently, the true prevalence of pathologic hemorrhoids is
not known. [2] In addition, although hemorrhoids are responsible for a large portion of anorectal
complaints, it is important to rule out more serious conditions, such as other causes of gastrointestinal
(GI) bleeding, before reflexively attributing symptoms to hemorrhoids. [3]
In a study of 198 physicians from different specialties, Grucela et al found the rate of correct
identification for 7 common, benign anal pathologic conditions (including anal abscess, fissure, and
fistula; prolapsed internal hemorrhoid; thrombosed external hemorrhoid; condyloma acuminata; and
full-thickness rectal prolapse) was greatest for condylomata and rectal prolapse and was lowest for
hemorrhoidal conditions. [4] There was no correlation between diagnostic accuracy and years of
physician experience. The investigators found the overall diagnostic accuracy among the physicians
to be 53.5%, with the accuracy for surgeons being 70.4% and that for the rest of the doctors being
less than 50%. [4]
Historical note
Hemorrhoidal symptoms have historically been treated with dietary modifications, incantations,
voodoo, quackery, and application of a hot poker. Molten lead has also been described as a treatment.
The adverse effects of these treatments have a direct relationship to whether patients relay persistent
or recurrent complaints to the clinician or return for further treatment.
For patient education information, see Hemorrhoids, Anal Abscess, Rectal Pain, and Rectal Bleeding.
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11/1/2017 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
Anatomy
Hemorrhoids are not varicosities; they are clusters of vascular tissue (eg, arterioles, venules,
arteriolar-venular connections), smooth muscle (eg, Treitz muscle), and connective tissue lined by the
normal epithelium of the anal canal. Hemorrhoids are present in utero and persist through normal
adult life. Evidence indicates that hemorrhoidal bleeding is arterial and not venous. This evidence is
supported by the bright red color and arterial pH of the blood.
Hemorrhoids are classified by their anatomic origin within the anal canal and by their position relative
to the dentate line; thus, they are categorized into internal and external hemorrhoids (see the following
image).
External hemorrhoids develop from ectoderm and are covered by squamous epithelium, whereas
internal hemorrhoids are derived from embryonic endoderm and lined with the columnar epithelium of
anal mucosa. Similarly, external hemorrhoids are innervated by cutaneous nerves that supply the
perianal area. These nerves include the pudendal nerve and the sacral plexus. Internal hemorrhoids
are not supplied by somatic sensory nerves and therefore cannot cause pain. At the level of the
dentate line, internal hemorrhoids are anchored to the underlying muscle by the mucosal suspensory
ligament.
Hemorrhoidal venous cushions are a normal part of the human anorectum and arise from subepithelial
connective tissue within the anal canal. Internal hemorrhoids have 3 main cushions, which are
situated in the left lateral, right posterior (most common), and right anterior areas of the anal canal.
However, this combination is found in only 19% of patients; hemorrhoids can be found at any position
within the rectum. Minor tufts can be found between the major cushions.
Present in utero, these cushions surround and support distal anastomoses between the superior rectal
arteries and the superior, middle, and inferior rectal veins. They also contain a subepithelial smooth
muscle layer, contributing to the bulk of the cushions. Normal hemorrhoidal tissue accounts for
approximately 15-20% of resting anal pressure and provides important sensory information, enabling
the differentiation between solid, liquid, and gas.
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External hemorrhoidal veins are found circumferentially under the anoderm; they can cause trouble
anywhere around the circumference of the anus.
Venous drainage of hemorrhoidal tissue mirrors embryologic origin. Internal hemorrhoids drain
through the superior rectal vein into the portal system. External hemorrhoids drain through the inferior
rectal vein into the inferior vena cava. Rich anastomoses exist between these 2 and the middle rectal
vein, connecting the portal and systemic circulations.
Most symptoms arise from enlarged internal hemorrhoids. Abnormal swelling of the anal cushions
causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the
suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal
mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood
oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge
(triggering pruritus) and predisposes to incarceration and strangulation.
Although many patients and clinicians believe that hemorrhoids are caused by chronic constipation,
prolonged sitting, and vigorous straining, little evidence to support a causative link exists. Some of
these potential etiologies are briefly discussed below.
Straining and constipation have long been thought of as culprits in the formation of hemorrhoids. This
may or may not be true. [5, 6, 7] Patients who report hemorrhoids have a canal resting tone that is
higher than normal. Of interest, the resting tone is lower after hemorrhoidectomy than it is before the
procedure. This change in resting tone is the mechanism of action of Lord dilatation, a surgical
procedure for anorectal complaints that is most commonly performed in the United Kingdom.
Pregnancy
Pregnancy clearly predisposes women to symptoms from hemorrhoids, although the etiology is
unknown. Notably, most patients revert to their previously asymptomatic state after delivery. The
relationship between pregnancy and hemorrhoids lends credence to hormonal changes or direct
pressure as the culprit.
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Portal hypertension has often been mentioned in conjunction with hemorrhoids. [8, 9, 10] However,
hemorrhoidal symptoms do not occur more frequently in patients with portal hypertension than in
those without it, and massive bleeding from hemorrhoids in these patients is unusual. Bleeding is very
often complicated by coagulopathy. If bleeding is found, direct suture ligation of the offending column
is suggested.
Anorectal varices are common in patients with portal hypertension. [11] Varices occur in the midrectum,
at connections between the portal system and the middle and inferior rectal veins. Varices occur more
frequently in patients who are noncirrhotic, and they rarely bleed. Treatment is usually directed at the
underlying portal hypertension. Emergent control of bleeding can be obtained with suture ligation.
Portosystemic shunts and transjugular intrahepatic portosystemic shunts (TIPS) have been used to
control hypertension and thus, the bleeding. [12]
Other risk factors historically associated with the development of hemorrhoids include the following:
Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate line and are
not innervated by cutaneous nerves. However, they can bleed, prolapse, and, as a result of the
deposition of an irritant onto the sensitive perianal skin, cause perianal itching and irritation. Internal
hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex
around the hemorrhoids. This spasm results in discomfort while the prolapsed hemorrhoids are
exposed. This muscle discomfort is relieved with reduction.
Internal hemorrhoids can also cause acute pain when incarcerated and strangulated. Again, the pain
is related to the sphincter complex spasm. Strangulation with necrosis may cause more deep
discomfort. When these catastrophic events occur, the sphincter spasm often causes concomitant
external thrombosis. External thrombosis causes acute cutaneous pain. This constellation of
symptoms is referred to as acute hemorrhoidal crisis and usually requires emergent treatment.
Internal hemorrhoids most commonly cause painless bleeding with bowel movements. The covering
epithelium is damaged by the hard bowel movement, and the underlying veins bleed. With spasm of
the sphincter complex elevating pressure, the internal hemorrhoidal veins can spurt.
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Internal hemorrhoids can deposit mucus onto the perianal tissue with prolapse. This mucus with
microscopic stool contents can cause a localized dermatitis, which is called pruritus ani. Generally,
hemorrhoids are merely the vehicle by which the offending elements reach the perianal tissue.
Hemorrhoids are not the primary offenders.
Pain results from rapid distention of innervated skin by the clot and surrounding edema. The pain lasts
7-14 days and resolves with resolution of the thrombosis. With this resolution, the stretched anoderm
persists as excess skin or skin tags. External thromboses occasionally erode the overlying skin and
cause bleeding. Recurrence occurs approximately 40-50% of the time, at the same site (because the
underlying damaged vein remains there). Simply removing the blood clot and leaving the weakened
vein in place, rather than excising the offending vein with the clot, will predispose the patient to
recurrence.
External hemorrhoids can also cause hygiene difficulties, with the excess, redundant skin left after an
acute thrombosis (skin tags) being accountable for these problems. External hemorrhoidal veins found
under the perianal skin obviously cannot cause hygiene problems; however, excess skin in the
perianal area can mechanically interfere with cleansing.
Epidemiology
Worldwide, the prevalence of symptomatic hemorrhoids is estimated at 4.4% in the general
population. In the United States, up to one third of the 10 million people with hemorrhoids seek
medical treatment, resulting in 1.5 million related prescriptions per year.
Patients presenting with hemorrhoidal disease are more frequently white, from higher socioeconomic
status, and from rural areas. There is no known sex predilection, although men are more likely to seek
treatment. However, pregnancy causes physiologic changes that predispose women to developing
symptomatic hemorrhoids. As the gravid uterus expands, it compresses the inferior vena cava,
causing decreased venous return and distal engorgement.
External hemorrhoids occur more commonly in young and middle-aged adults than in older adults.
The prevalence of hemorrhoids increases with age, with a peak in persons aged 45-65 years.
Prognosis
Most hemorrhoids resolve spontaneously or with conservative medical therapy alone. However,
complications can include thrombosis, secondary infection, ulceration, abscess, and incontinence. The
recurrence rate with nonsurgical techniques is 10-50% over a 5-year period, whereas that of surgical
hemorrhoidectomy is less than 5%.
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Clinical Presentation
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Back to List
Author
Scott C Thornton, MD Associate Clinical Professor of Surgery, Yale University School of Medicine;
Director, Colorectal Teaching, Bridgeport Hospital; Private Practice, Park Avenue Surgical Associates
Scott C Thornton, MD is a member of the following medical societies: American Society of Colon and
Rectal Surgeons
Coauthor(s)
Kyle R Perry, MD is a member of the following medical societies: American Medical Association,
Michigan State Medical Society, Emergency Medicine Residents' Association
Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency
Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical
Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
William G Gossman, MD, FAAEM Associate Clinical Professor of Emergency Medicine, Creighton
University School of Medicine; Chairman, Department of Emergency Medicine, Creighton University
Medical Center
William G Gossman, MD, FAAEM is a member of the following medical societies: American Academy
of Emergency Medicine
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
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11/1/2017 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
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
Additional Contributors
Brian J Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of
Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center
College of Medicine
Brian J Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies:
American Association for the Surgery of Trauma, Eastern Association for the Surgery of Trauma,
Southern Surgical Association, American College of Chest Physicians, American College of Surgeons,
American Medical Association, Association for Academic Surgery, Association for Surgical Education,
Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Tennessee
Medical Association
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous
authors David R Gurley, MD, Richard Sinert, DO, and Pilar Guerrero, MD,to the development and
writing of a source article.
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