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Anorectal conditions can be approached using an algorithm that addresses the presence or absence of pain, bleeding, swelling, and pruritus, in combination with an assessment of the patient’s overall health (see Fig. 82.2 ).
Patients who seek treatment for nonspecific anorectal complaints should be evaluated for the presence of underlying systemic disease (e.g., cancer, diabetes mellitus, immunodeficiency) because disorders of the anorectum may be the initial presentation of associated conditions.
Patients with a sexually transmitted disease (STD) should be evaluated for HIV infection, use of the anus for sexual purposes, and the possibility of domestic violence or abuse.
Most anorectal conditions can be symptomatically improved by adherence to the WASH regimen ( w arm water, a nalgesics, s tool softeners, h igh-fiber diet).
Thrombosed external hemorrhoids are covered by modified anoderm and may be excised and drained within 48 hours of formation. After 48 hours, the clot begins to dissolve, and conservative management with the WASH regimen is indicated.
Internal hemorrhoids are covered with mucosa and should be referred to a colorectal surgeon for definitive management.
Acutely thrombosed, gangrenous fourth-degree internal hemorrhoids require urgent surgical consultation.
Fistulous tracts should not be probed.
Pilonidal abscesses should be drained with needle aspiration or with a longitudinal incision off the midline.
Pruritis ani is caused by a variety of conditions, including infection, hemorrhoids, topical irritants, cutaneous conditions, cancer, and hypersensitivity to foods and drugs (see Box 82.5 ).
Sensitivity is required when managing patients with anorectal foreign bodies. Health care provider safety is imperative when evaluating foreign bodies with sharp edges.
Distal anorectal foreign bodies often can often be removed in the ED, whereas proximal or sharp ones should be removed in the operating room.
Patients visit the emergency department (ED) with a variety of anorectal complaints. Particular focus on sensitivity and a professional demeanor is important in these interactions, because patients may find it challenging to discuss historical details openly and to describe physical complaints related to this area of the body and its function.
The anorectum begins at the rectosigmoid junction at the level of the third sacral vertebra (S3). The rectum follows the sacral curvature for 12 to 15 cm and then sharply turns posteriorly and inferiorly at the puborectalis muscle ( Fig. 82.1 ). Here the anal canal begins its 4-cm course to the anus, which is supported by three muscle groups—levator ani and the internal and external anal sphincters. Anal valves and crypts with mucous glands for lubrication are located 2 cm proximal to the anal verge at the dentate line. Proximal to the crypts are the columns of Morgagni, where the epithelium of the anal canal changes from pink columnar (as in the rectum) to squamous.
The superior, middle, and inferior hemorrhoidal arteries provide blood supply to the anorectum. They arise from the inferior mesenteric, internal iliac, and internal pudendal arteries, respectively. The superior hemorrhoidal veins drain into the portal system, and the inferior hemorrhoidal veins drain into the caval system. Lymphatic drainage is to the inferior mesenteric nodes above the dentate line and to the inguinal nodes from all areas of the anorectum.
Sympathetic and parasympathetic nervous systems function together to retain the contents of the rectum until evacuation is desired. Sympathetic fibers from L1 to L3 (upper rectum) and presacral nerves (lower rectum) inhibit the contraction of rectal smooth muscle, and L5 fibers cause the internal sphincter to contract. Elimination occurs when parasympathetic fibers from the anterior roots of S2 to S4 cause the rectal wall to contract and the internal sphincter to relax. Voluntary external sphincter control is mediated by motor branches of the pudendal nerve (S2, S3) and the perineal branch of S4. The levator ani is supplied by the pudendal nerve and pelvic branches of S3 to S4 fibers. Sensory perception of rectal distention relies on parasympathetic fibers from S2 to S4. The abundant sensory nerve endings of the distal anal epithelium transmit via the pudendal nerve.
Defecation begins as the rectum becomes distended, the internal sphincter relaxes, and stool enters the anal canal. At an appropriate time and place, the external sphincter relaxes to complete the process of elimination. When voluntary straining is required, abdominal muscles contract, the rectal angle straightens, and the pelvic floor descends. To postpone defecation, the external sphincter contracts voluntarily, relaxing the rectal wall and quelling the urge to defecate unless there is an underlying sphincter disorder or an overwhelming volume of stool.
A history of anorectal and gastrointestinal (GI) symptoms, as well as underlying systemic conditions, elucidate the diagnosis of most anorectal disorders ( Box 82.1 ; Fig. 82.2 ). Common complaints include bleeding, swelling, pain, itching, and discharge. History includes questions about onset, duration, and quality of symptoms, and details of bowel habits (changes in color, frequency, or consistency of the stool and the presence of straining, flatus, or incontinence of solid or liquid stool). Sexual practices or history of radiation exposure are also relevant in most cases. Underlying GI disorders (e.g., Crohn’s disease, cancer, polyps) often produce atypical presentations and patients with an underlying systemic disease such as AIDS, cancer, diabetes mellitus, or coagulopathy may develop more severe complications of standard anorectal conditions.
Pain
Bleeding
Swelling
Itching
Discharge
Urgency
Change in bowel habits (straining, flatus, color, consistency, frequency)
Nausea or vomiting
Incontinence of stool
Underlying GI disease (Crohn’s disease, cancer, polyps)
Diabetes mellitus
Coagulopathy
Cancer
HIV infection
Penetration
Known STDs
Assault
In patients presenting with rectal bleeding, the color, amount, and relationship to defecation are essential factors. Pain and bright red blood are consistent with anal fissures or hemorrhoids. Fissure pain is sharp, sudden in onset, and is not associated with swelling, whereas pain from a prolapsed or thrombosed hemorrhoid is gnawing, continuous, and more gradual in onset. Painless rectal bleeding may occur with internal hemorrhoids, cancer, or precancerous lesions. Red blood on the toilet paper usually is caused by anal fissures or external hemorrhoids, though minute quantities can result from any irritating condition. Bright red blood that drips into the toilet bowl or streaks around the stool is frequently caused by internal hemorrhoids. Blood mixed with stool typically originates above the rectum, whereas melena indicates an upper GI source, proximal to the ligament of Treitz. Bloody mucus is associated with cancer, inflammatory bowel disease, and proctitis.
Patients who experience perianal swelling or have the sensation of rectal fullness often list hemorrhoids as their chief complaint. Painful swelling that bleeds is usually a thrombosed hemorrhoid, but abscesses, pilonidal disease, and hidradenitis suppurativa should be considered. Painless, itchy swelling may be caused by condylomata acuminata or secondary syphilis. A mass protruding through the anal orifice may signal rectal prolapse or cancer ( Fig. 82.3 ).
Severe, episodic anorectal pain that is not associated with bleeding or swelling may represent proctalgia fugax or levator ani syndrome. Perianal itching (pruritus ani) is caused by poor hygiene or any lesion that makes it difficult to clean the perineum, or may result from exposure to certain foods or medications.
The physical examination should ensure the patient’s comfort and privacy. With the patient in the lateral decubitus position and partially covered with a sheet, inspect the buttocks and anal orifice. Note elements of personal hygiene and anatomic disruptions, such as fissures, skin tags, protruding hemorrhoids, abscesses, or other lesions. Ask the patient to strain and note the integrity of the pelvic floor, prolapse of hemorrhoids, or rectal mucosa. Placing the fingertips of both hands along either side of the anus, as close to the anal verge as possible, and applying gentle outward traction allows the anus to be slowly everted, which often reveals anal abnormalities. If the area is slippery, placing 4-by-4-inch gauze pads under the fingers will facilitate sufficient traction. A digital rectal examination begins by placing a well-lubricated gloved finger flat against the anal opening and exerting gentle pressure until the external sphincter relaxes, allowing the finger to enter the anus. Assess anal sphincter tone by asking the patient to squeeze the anal muscles against the examining finger. Accessible areas of the anorectum are examined for masses and areas of tenderness with a circumferential sweep. The cervix or prostate is palpated through the rectal wall. On withdrawal, the contents on the glove are assessed for frank or occult blood, mucus, or pus.
If desired, direct visualization of the anus may be accomplished by anoscopy. A lubricated anoscope is inserted into the anus, with the obturator in place. When the obturator is removed, the area can be viewed for sites of bleeding, hemorrhoids, masses, or abnormal tissue, as well as the dentate line and anal epithelium.
Hemorrhoids occur when the three anal vascular submucosal cushions become engorged. Blood supply arises from the arterial system, causing hemorrhoidal bleeding that is bright red. The muscularis submucosa cushions the anal canal during defecation and aids fecal continence. As the supportive tissue deteriorates, the veins draining the area become distended and prolapse through the anal orifice, which may result in bleeding and/or thrombosis. Some controversy exists about whether straining and constipation cause these changes by producing venous backflow when intra-abdominal pressure increases. A familial predisposition is recognized, but whether this is a result of genetics or acquired factors such as diet is unknown. Direct pressure on a hemorrhoidal vein can produce symptomatic hemorrhoids in pregnant women, and thrombosed hemorrhoids are associated with prolonged labor or deliveries that result in traumatic tears.
Hemorrhoids are not varicose veins; rather, they are normal structures that manifest symptoms when the muscularis submucosa weakens and the anal cushions are displaced distally. Conditions that increase sphincter tone correlate with a higher prevalence of hemorrhoids. Portal hypertension does not typically cause hemorrhoids in adults, although it appears to be a cause in children. Bleeding in patients with portal hypertension may be caused by rectal varices, which are vascular communications between the superior and middle hemorrhoidal veins.
Patients often refer to any perianal condition as “hemorrhoids.” Bleeding with defecation is the most common complaint and, unless the hemorrhoids are thrombosed, is typically painless. Patients report variable amounts of bright red blood on toilet paper when wiping or in the toilet bowl. Many complain of swelling, itching, mucoid discharge, or a moist perianal area. History should address recent stool patterns such as diarrhea or constipation, chronic medical problems such as portal hypertension or bleeding disorders, and a dietary and family history. Frequent bowel movements, prolonged sitting, heavy lifting, and straining while defecating exacerbate symptoms.
Physical examination should ascertain the type and degree of hemorrhoids by visual inspection at rest and during straining. Nonprolapsing hemorrhoids can be visualized on anoscopy as a focus of bleeding or as they bulge when the patient is asked to strain. Anoscopy is painful and not useful in cases of prolapsed or thrombosed hemorrhoids ( Table 82.1 ). Table 82.2 shows the classification of hemorrhoids based on history, physical findings, and reducibility.
Type | Origin | Epithelium |
---|---|---|
External | Inferior hemorrhoidal plexus | Modified squamous epithelium (anoderm) |
Below the dentate line | ||
Internal | Superior hemorrhoidal plexus | Transitional or columnar epithelium (mucosa) |
Above the dentate line | ||
Mixed | Superior and inferior hemorrhoidal plexus | Transitional, columnar, or modified squamous epithelium (mucosa and anoderm) |
Type | Prolapse | Mode of Reduction | Treatment |
---|---|---|---|
First degree | None | N/A | Medical |
Second degree | During defecation | Spontaneous | Medical |
Third degree | May be spontaneous or during defecation | Manual | Medical Optional surgical repair |
Fourth degree | Permanent | Irreducible | Surgical repair |
The symptoms of nonthrombosed external and nonprolapsing internal hemorrhoids can be ameliorated by a standard regimen, WASH ( w arm water, a nalgesics, s tool softeners, and h igh-fiber diet) aimed at combating the problems that led to their formation ( Box 82.2 ). Anal canal pressures decrease in very warm water (40°C [104°F]—about the temperature of a well-heated “hot tub” or spa). Patients can direct a shower stream at the area for several minutes or take sitz baths. This can facilitate spontaneous reduction of prolapsed hemorrhoids or other tissue and can ease the discomfort arising from tightly constricted musculature. Drinking water helps produce a softer stool. Mild oral analgesic agents such as acetaminophen or nonsteroidal antiinflammatory drugs (NSAIDs) reduce pain. Passage of stool is more comfortable with stool softeners and fiber supplementation with psyllium (e.g., Metamucil©), one to two rounded teaspoons in eight ounces of water once a day, or a high-fiber diet (20–30 g of dietary fiber/day). Several over-the-counter preparations are available for the treatment of hemorrhoidal symptoms; their use improves hygiene and provides temporary symptom relief rather than correction of the condition. Topical anesthetics, corticosteroids, astringents (e.g., witch hazel), mineral oils, and cocoa butter are often applied as temporary soothing agents, although there is no evidence to support their use or the relative benefits of one over the other. Astringents may promote better hygiene and reduce discomfort by preventing residual stool from further irritating the hemorrhoids. Lipophilic agents provide a smooth and greasy coating that can prevent the adherence of stool to the irritated areas and can promote a slippery pathway during defecation. We do not recommend use of topical corticosteroids beyond a few days because of risk of atrophic skin changes.
W arm water
A nalgesic agents
S tool softeners
H igh-fiber diet
Patients with second- or third-degree internal hemorrhoids benefit from the WASH regimen and may be discharged from the ED. Permanent resolution of symptoms may require surgical banding, sclerotherapy, or elective hemorrhoidectomy ( Table 82.3 ). Patients with acute, gangrenous, thrombosed fourth-degree internal hemorrhoids may require emergent hemorrhoidectomy.
Classification | Management |
---|---|
Thrombosed external hemorrhoids | Excision in emergency department |
Second- and third-degree internal hemorrhoids | Elective surgical repair Banding Sclerotherapy Hemorrhoidectomy |
Fourth-degree hemorrhoids (nonthrombosed) | Nonemergent hemorrhoidectomy |
Thrombosed or gangrenous fourth-degree internal hemorrhoids | Emergent hemorrhoidectomy |
Acutely thrombosed external hemorrhoids can be excised ( not incised and drained) to provide relief within the first 72 hours after the onset of symptoms ( Fig. 82.4 ). Although incision may help to relieve pain in the short term, it results in incomplete evacuation of the clot, subsequent rebleeding, swelling, and formation of a skin tag. If not excised, a thrombosed external hemorrhoid resolves spontaneously after several days when it ulcerates and leaks the dark accumulated blood. Residual skin tags may persist, making anal hygiene more challenging. In the ED setting, this procedure is not commonly performed in pediatric patients, pregnant women, or immunocompromised patients.
Nonsurgical therapy with topical nifedipine (0.2%) and lidocaine (1.5%) gel applied twice daily for a few days may alleviate symptoms in some patients. Although not widely used, the purported effectiveness of this regimen is related to the ability of nifedipine to modulate resting sphincter tone and thereby reduce the associated pain and inflammation.
The development of an anal fissure is the most common cause of intensely painful rectal bleeding of sudden onset. A superficial tear in the anoderm results when a hard piece of feces is forced through the anus, usually in patients who are constipated, or may occur during sexually related anal instrumentation. It is the most commonly encountered anorectal problem in pediatric patients, especially infants. Most fissures occur along the posterior midline, where the skeletal muscle fibers that encircle the anus are weakest. Anterior midline fissures are more common in women than in men. Fissures that occur elsewhere may be associated with systemic diseases such as leukemia, Crohn’s disease, human immunodeficiency virus (HIV) infection, tuberculosis (TB), or syphilis. If the fissure does not resolve promptly, the classical so-called fissure triad of deep ulcer, sentinel pile, and enlarged anal papillae may develop ( Fig. 82.5 ). A sentinel pile forms when the skin at the base of the fissure becomes edematous and hypertrophic; it can form a permanent skin tag and underlying fistulous tract.
The patient with an anal fissure reports sudden, searing pain during defecation that may be accompanied by a small amount of bright red blood on the stool or toilet paper. This is followed by a nagging, intermittent or constant burning sensation caused by internal sphincter spasm. Subsequent bowel movements are often quite painful and the external sphincter may exhibit a reflex spasm. A physical examination must be performed cautiously to avoid perpetuating the cycle of spasm and pain. If the patient can tolerate it, gentle anal eversion, as described above, often reveals the culprit fissure. The depth of the fissure, its orientation to the midline, and the presence of a coexisting sentinel pile should be noted. A digital rectal examination during an acute exacerbation often is challenging because of pain and sphincter spasm.
We recommend a trial of conservative treatment with the WASH regimen (see Box 82.2 ), which focuses on eliminating constipation with a bulking agent, stool softener, and high-fiber diet. For severe discomfort, one to three days of topical anesthetic gel may be helpful. Specific measures for the treatment of anal fissures that do not resolve with conservative therapy are summarized in Box 82.3 and are often employed during follow-up visits with the patient’s primary care provider or specialist. Parental encouragement of pediatric patients helps prevent encopresis, which can result from a fear of painful bowel movements. Most acute uncomplicated fissures resolve in 2 to 4 weeks.
WASH regimen a
a See Box 86.2
Nitroglycerin ointment (0.4%) bid or tid
Nifedipine gel (0.2%) bid with lidocaine (1.5%)
Botulinum toxin (surgical consultation)
Anal dilation performed with the patient under general anesthesia
Surgical excision
For adult patients with recurring anal fissures, application of various topical agents aimed at reducing sphincter pressures and local pain may be effective. There is not uniform consensus for any of these treatments, however, some gastroenterologists and colorectal surgeons report that some individuals may benefit. It would be prudent to consult with the patient’s ongoing provider to determine if one of these drug therapies is favored. Nitroglycerin ointment applied topically to the anoderm 2 or 3 times daily may relieve the pain but may cause a vasodilatory headache. Nifedipine gel (0.2%) in combination with lidocaine (1.5%) applied to the anal area twice daily is effective in promoting healing and reducing discomfort in the management of anal fissures by reducing anal canal pressures through local calcium channel blockade. Referral to a colorectal surgeon for definitive management may include injection of botulinum toxin, anal dilation, or sphincterotomy in patients who do not respond to conservative therapy. ,
Anorectal abscesses and subsequent fistulae occur in otherwise healthy adults when the mucus-producing glands at the base of the anal crypts occlude. In most cases, this is simply a functional collection of excess thick mucus, however, sometimes abscesses may result from intrarectal or penetrating trauma, or herald the presence of inflammatory bowel disease, cancer, radiation injury, or infection (TB, lymphogranuloma venereum, actinomycosis). Common causative bacteria are Staphylococcus aureus, Escherichia coli, Streptococcus, Proteus, and Bacteroides.
Anorectal abscess is an acute disease that naturally progresses to fistula formation in the body’s attempt to drain the infection spontaneously. Symptoms vary depending on the site of infection, but incision and drainage constitute curative treatment ( Table 82.4 ). Delays may allow extension of the infection and eventual compromise of the sphincter mechanism. Adjunctive antimicrobial therapy is indicated in patients who are immunocompromised, diabetic, or have valvular heart disease. One-third of patients with AIDS develop anorectal abscesses and fistula. In these patients, antibiotic therapy choices should be guided by the patient’s immune status in consultation with infectious disease specialists who are familiar with local antibiograms. HIV-infected patients are prone to having incomplete fistulous tracts, which impedes spontaneous drainage, highlighting the urgency of treating these patients promptly.
Feature | Perianal | Ischiorectal | Intersphincteric | Supralevator | Postanal |
---|---|---|---|---|---|
Incidence | 40%–45% | 20%–25% | 20%–25% | <5% | 5%–10% |
Location | Outside and verge | Buttocks | Lower rectum | Above levator ani | Deep to external sphincter |
Symptoms | Painful perianal mass | Buttock pain | Rectal fullness | Perianal and buttock pain | Rectal fullness, pain near coccyx |
Fever, ↑ WBCs | − | ± | ± | + | + |
Associated fistula | ++ | + | +++ | +++ | − |
ED incision and drainage | + | ± | − | − | − |
Sites of anorectal abscess formation are depicted in Fig. 82.6 . Early diagnosis may be difficult because pain often precedes physical findings of a mass or fluctuance.
Perirectal and perianal abscesses account for about half of anorectal abscesses. They produce painful swelling at the anal verge that is worsened by defecating or sitting. Most patients are afebrile and have localized tenderness, erythema, swelling, and fluctuance that is particularly obvious on examination with palpation between the index finger (from within the rectum) and the thumb (through the outside skin). ED management by incision and drainage may be possible in patients without comorbidities (e.g., diabetes mellitus, extremes of age, compromised immune status), but the procedure can be very painful and often requires procedural sedation and/or field block with local anesthesia. The WASH regimen (see Box 82.2 ) may alleviate postprocedure discomfort. Antibiotics generally are unnecessary following incision and drainage of uncomplicated superficial abscesses in healthy adult patients, except in cases involving associated cellulitis. There is emerging evidence that adjuvant antibiotics may help reduce the likelihood of subsequent fistula formation, even in patients without cellulitis. In consultation with infectious disease specialists at individual institutions to address local antibiograms and the prevalence of methicillin-resistant Staphylococcus aureus (MRSA), one could consider administering one or more of the following: cephalexin 500 mg PO bid-qid; sulfamethoxazole/trimethoprim (800 mg/160 mg PO Q12 hours; doxycycline 100 mg PO bid.
Ischiorectal abscesses account for one-fifth to one-quarter of anorectal abscesses. They form outside the sphincter muscles in the buttocks, and patients generally present complaining of severe pain. The diagnosis is evident if an indurated mass is seen on the buttocks but sometimes the abscess is deep in the tissue and not externally identifiable. Patients may have fever and/or leukocytosis. Ultrasound may be useful to localize fluid collections and guide aspiration, particularly if there is no significant induration. Although most of these abscesses will require drainage performed with the patient under general anesthesia, superficial abscesses can be treated in the ED. If the patient is febrile, we recommend a short course of antibiotics, such as cefazolin 1 g IM or IV administered before drainage, followed by cephalexin 500 mg orally qid for 5 to 7 days.
One-fourth of abscesses form in the intersphincteric space, located deep to the external sphincter and inferior to the levator ani. The infection tracks cephalad and may appear to be a mass in the rectum and can be confused with a thrombosed internal hemorrhoid. Patients report continuous rectal pressure and a throbbing pain exacerbated by defecation or sitting. These patients also may have fever and/or leukocytosis which are neither sensitive nor specific signs. External evidence of inflammation may be lacking, but a rectal examination reveals an indurated, and sometimes draining mass. Associated fistulae and inguinal lymphadenopathy are common. Surgical consultation and advanced imaging, such as CT scan or fistulogram, are necessary to evaluate and treat the entire abscess and fistula network.
Supralevator abscesses, which cause less than 5% of anorectal abscesses, present as perianal and buttock pain associated with fever and frequently, an associated leukocytosis. External evidence is usually absent, which often leads to a delay in accurate diagnosis. Patients are often obese or have diabetes, Crohn disease, pelvic inflammatory disease, or diverticulitis. A tender mass may be palpated on rectal or pelvic examination, but the abscess is often discovered on CT scan performed to evaluate the patient with significant symptoms but no identified cause. Emergent surgical treatment is indicated to drain the abscess and excise the fistulous network.
Postanal abscesses are uncommon and occur posterior to the rectum, deep to the external sphincter and inferior to the levator ani. Patients experience severe rectal discomfort and coccygeal pain. They usually are febrile and have continuous pain that does not change with position. A rectal examination is painful, and anal drainage is rare. Many of these abscesses are missed on initial presentation, unless a CT scan is performed. These abscesses require surgical consultation and management.
A large, communicating, horseshoe-shaped abscess may form in the ischiorectal, intersphincteric, or supralevator spaces. The extent of these abscesses is identified by CT scan and surgical management is necessary.
A delay in the management of an anorectal abscess may lead to the destruction of surrounding tissue, especially in diabetic or immunocompromised patients. Extensive cellulitis, necrotic tissue, or identification of gas on radiography suggest the possibility of necrotizing fasciitis, Fournier gangrene, or tetanus. Treatment is described in Chapter 126 , and includes timely, wide surgical débridement, administration of intravenous antibiotics with anaerobic coverage such as a combination of piperacillin (4.5 gm IV q8h), vancomycin (15 to 20 mg/kg q8h to q12h), and clindamycin (900 mg IV q8h), and tetanus prophylaxis.
A fistula is a connection between two epithelium-lined surfaces and commonly develops in patients with abscesses. Other causes include Crohn’s disease, trauma, foreign body reactions, TB, and cancer. The anorectal complaint may be the presenting symptom of the underlying disease. Patients notice a recurrent or persistent perianal discharge that becomes painful when one of the openings becomes occluded. A digital rectal examination may reveal a tract in the perineum or canal. Probing of fistulous tracts is not recommended because the danger of creating a new tract outweighs the benefit of identifying the path of the existing fistula. Spontaneous resolution of fistula-in-ano is rare.
Although symptoms may resolve when antibiotics are administered, they commonly return when therapy is discontinued. Definitive treatment of the fistulous network at the time of incision and drainage of the abscess prevents the ongoing progression of the disease. Fistulectomy or application of fibrin glue are commonly accepted practices of adult and pediatric colorectal surgeons. New treatments that are underway include the use of biomaterials (e.g., platelet rich plasma) and laser closure techniques.
Abscesses containing hair and pus in the midline of the sacrococcygeal area afflict young adults with a 4:1 male predominance and are more common in obese and hirsute persons. Many of those who develop this disease have evidence of midline hair growth in other areas of the body, such as eyebrows that connect with each other. Pilonidal disease occurs more commonly in people who sit for long periods, and was first identified as “Jeep driver’s disease” during World War II. The disease is rare after 40 years of age, even for those who were affected in their youth, and should not be confused with anal fistulae, perirectal abscesses, hidradenitis suppurativa, or granulomatous diseases (e.g., syphilis, TB). Pilonidal disease is believed to arise when bacteria enter the usually sterile hair follicle and produce inflammation and edema, thereby occluding the opening to the skin surface. The contents expand until the hair follicle ruptures, and the material spreads into the surrounding subcutaneous fatty tissue, where a foreign body reaction leads to abscess formation. The purulent material subsequently spreads to the presacral skin through an epithelialized tract. In those with chronic or recurrent disease, visible or palpable tracts containing hair and cellular debris may be identified.
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