ANORECTAL DISORDERS*

ANORECTAL DISORDERS*

GASTROINTESTINAL EMERGENCIES, PART I1 0733-8627/96 $0.00 + .20 ANORECTAL DISORDERS David M. Janicke, MD, PhD, and Mark R. Pundt, MD HEMORRHOIDS A...

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GASTROINTESTINAL EMERGENCIES, PART I1

0733-8627/96 $0.00

+ .20

ANORECTAL DISORDERS David M. Janicke, MD, PhD, and Mark R. Pundt, MD

HEMORRHOIDS

A review by Johanson and S ~ n n e n b e r gof~ ~the National Health Interview Surveys for the United States from 1983 to 1986 revealed a prevalence of hemorrhoidal complaints of 4.4% as self-reported by patients. Patients who complain of "hemorrhoids" (being the most familiar and frequent anorectal problem), however, commonly have in reality other anorectal pathology52that cannot be differentiated by symptoms alone. The prevalence of hemorrhoids is equal between the sexes; however, men are more likely to seek treatment. The prevalence of hemorrhoids increases with age until the seventh decade, at which time there is a slight A common predisposing factor to the development of hemorrhoids is pregnancy.53Other earlier reported predisposing factors such as constipation and portal hypertension have been shown not to 3s, 39, 41 be associated with an increase in hemorrhoidal

Etiology and Pathophysiology Internal and external hemorrhoids are anatomically defined based on their origin in the anal canal above or below the dentate line (embryonic endoderm and ectoderm fusion site), re~pectively.~~ Internal hemorrhoids are covered with anal mucosa (simple columnar epithelium) The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, the Department of Defense, or the US Government.

From the Department of Emergency Medicine, State University of New York at Buffalo, Millard Fillmore Hospitals, Buffalo, New York

EMERGENCY MEDICINE CLINICS OF NORTH AMERICA ~~

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VOLUME 14 * NUMBER 4 NOVEMBER 1996

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lacking sensory innervation, whereas external hemorrhoids are covered with anoderm (stratified squamous epithelium), with sensory innervation via the inferior rectal nerve. Venous drainage of the internal hemorrhoidal plexus superior to the dentate line is predominately via the superior rectal vein, which drains into the portal system. Inferior to the pectinate line, the external hemorrhoidal plexus is drained via the inferior rectal vein, which drains into the vena cava. Anastomoses exist between all three rectal veins.57Figure 1 shows the pertinent anatomy of the anorectum. The exact pathogenesis of hemorrhoids is not known. The theory that hemorrhoids are simply varicosities of the hemorrhoidal vein plexuses is probably incorrect.21, 49 Hemorrhoids are thought to be secondary to the distal displacement of the anal cushions into the anal canal. Anal cushions (usually three in number) are located circumferentially around the anal canal (above the dentate line); contain blood vessels, smooth

ANOD€d

INTERSPHINCIEPIC LtNf 6WQf IlNf

0):

HlOONj INTERMUSCULAR GWOV€>

Figure 1. Anatomy of the anorectum. (From The ClBA Collection of Medical Illustrations by Frank H. Netter, MD, 1962; with permission.)

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muscle, and supportive connective tissue; and are thought to be normal anatomy.21, 49 Increased measured maximum resting anal pressure has been the most consistently reported physiologic abnormality associated with hemorrhoid^.^^ Internal hemorrhoids are graded based on the degree of prolapse of the hemorrhoidal tissue into the anal canal and out of the anus. Firstdegree hemorrhoids project into the anal canal but do not prolapse. Second-degreehemorrhoids protrude on defecation but return spontaneously with cessation of straining. Third-degree hemorrhoids protrude with straining and are persistent, requiring intermittent manual reduction. Fourth-degree hemorrhoids have irreducibly prolapsed out of the anus.21, 75 A thrombosed external hemorrhoid or perianal hematoma is a tender bluish mass located in the anal canal just proximal to the anal verge. Although the pathology has been reported to be thrombosis within a vessel or formation of a hematoma, one histopathologic study denounces both these mechanisms and suggests that the pathology is secondary to clotting of blood within a venous saccule of the hemorrhoidal venous plexus and would be more appropriately termed a clotted venous s a c c ~ l e . ~ ~ Clinical Presentation and Diagnosis

The most frequent cause of hematochezia is hemorrhoids.6,21 Bleeding from hemorrhoids is usually painless and associated with defecation; blood is bright red in color, not admixed with the stool, and varies in amount from streaks on toilet tissue to frank blood in the commode. Internal hemorrhoids are above the pectinate line and are usually painless. In contrast, patients with an acutely thrombosed external hemorrhoid will complain primarily of pain, with bleeding being present infrequently. Hemorrhoidal symptoms can also include patient identification of a mass, swelling, burning, and pruritis. Mucoid drainage may also be noted, most commonly with permanently prolapsed internal hemorrhoid^.'^, 15,

23, 55

A thorough history along with a physical examination that includes anoscopy will usually confirm the diagnosis. On digital rectal examination, internal hemorrhoids are usually not tender and not palpable unless they have prolapsed or thrombosed. Examination by anoscopy will reveal even nonprolapsing internal hemorrhoids and, by having the patient strain, the size and degree of prolapse can be assessed. Stroking the surface of an internal hemorrhoid with a cotton-tipped applicator during anoscopy may demonstrate bleeding. External hemorrhoids, especially when they are thrombosed, are easy to identify as an enlarged,

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painful, bluish mass at the anal verge. External skin tags may also be noted around the anal verge representing old thrombosed external hemorrhoid^.^, 13, 23

Treatment and Disposition Thrombosed External Hemorrhoids

Painful symptoms from a thrombosed external hemorrhoid are most acute over the first 48 to 72 hours, with symptoms resolving over a 7to 10-day period of time. Surgical excision of a thrombosed external hemorrhoid is reserved for patients presenting during the first 48 to 72 hours after the onset of acute painful symptoms, or if ulceration or rupture has occurred, or if medical treatment has failed and chronic symptoms persist. If the patient is seen more than 48 to 72 hours after the onset of pain, medical treatment consisting of sitz baths twice a day, stool softeners, and analgesics, both systemic and topical, are usually effective.9,23. 29. 55, 75 The procedure for surgical excision of a thrombosed external hemorrhoid is as follows: following infiltration of the hemorrhoidal area with a local anesthetic, an eliptical incision is made and the thrombosed hemorrhoid is excised along with the wedge of the overlying skin (Fig. 2). The incision should not extend under the cutaneous layer or past the anal verge. It is recommended that a long-acting anesthetic, such as bupivacaine 0.5% with epinephrine (1:200,000), be used for local anesthesia and that the anesthetic be alkalinized with sodium bicarbonate to decrease the burning pain on infiltrati~n.~, 23, 24, 29 Postoperative care should include pressure dressing and bed rest at home for a few hours, a stool softener, frequent sitz baths, and systemic and topical analgesia. Patients should have at least one postoperative evaluation in 48 to 72 hours. Possible complications include development of infection with resulting abscess or fistula formation and recurrence of clot over a few days9,24 A possible promising treatment for the pain associated with thrombosed hemorrhoids is the use of nitroglycerin ointment applied circumferentially to the external anus and distal anal canal. This has been shown to successfully relieve pain in the small number of patients studied, who presented 2 to 4 days after onset of symptoms. It is hypothesized that nitroglycerin acts to diminish the pain by decreasing internal sphincter spasm, which has been shown to be associated with thrombosed external hemorrhoid^.^^

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Figure 2. Excision of a thrombosed external hemorrhoid. A, The area is infiltrated with 0.5% bupivacaine in 1 : 200,000 epinephrine. B and C, An eliptical incision is made and the thrombosed hemorrhoid is excised along with a wedge of skin. D, Skin edges are sufficiently separated to permit adequate drainage, thereby preventing reaccumulation of a clot. (From Corman ML: Hemorrhoids. In Colon and Rectal Surgery, ed 3. Philadelphia, JB Lippincott, 1993, p 79; medical illustrator is L. Barnes; with permission.)

Internal Hemorrhoids

The treatment of internal hemorrhoids is based on the degree of internal hemorrhoid and the patient’s symptoms. In patients with minor symptoms (e.g., intermittent bleeding, prolapsing but a reducible mass) from internal hemorrhoids, initial conservative medical treatment can be used. Treatment should consist of high-fiber diet, adequate fluid intake, sitz baths, stool softeners, proper anal hygiene, and topical steroids. Nonthrombosed prolapsed hemorrhoids should be manually reduced, and conservative treatment should be initially used. The patient should be given a gastroenterology or surgical follow-up referral for possible

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more definitive treatment and further evaluation of rectal bleeding (eg., rectosigmoidoscopy).9~ 15, z3, 55 If a patient presents with a painful and edematous incarcerated fourth-degree hemorrhoid, reduction following local anesthetic infiltration can be attemptedz3and surgical consult should be obtained in the emergency department.13, Incarcerated hemorrhoids are associated with severe pain, possible tissue necrosis and severe infection, and urinary retention. Incarcerated hemorrhoids must be differentiated from rectal prolapse. If an internal hemorrhoid needs more definitive treatment, most commonly this will be accomplished by means other than surgical hemorrhoidectomy. Various nonsurgical modalities have been used for the treatment of internal hemorrhoids including sclerotherapy, rubber band ligation, infrared coagulation, bipolar electrocoagulation, and laser therapy. These methods are usually not performed in the emergency department but referred for surgical or gastroenterology consultation. All of the above methods are used for first-degree and second-degree hemorrhoids; however, rubber band ligation and laser therapy have also been used for higher-degree hemorrhoids.Q 75 Meta-analysis comparing rubber band ligation, infrared coagulation, and injection sclerotherapy shows that rubber band ligation exhibits greater long-term efficacy but is also associated with a greater incidence of postoperative pain.40Following rubber band ligation patients may present 7 to 10 days postoperatively with rectal bleeding secondary to sloughing of the hemorrhoid. Patients presenting with anorectal pain, fever, or urinary retention 2 to 7 days after rubber band ligation should be evaluated for perianal sepsis which has been reported in a small number of cases.7,65, 71 Practice guidelines presented by the American Society of Colon and Rectal Surgeons75recommend that surgical hemorrhoidectomy is indicated if (1) conservative (e.g., sclerotherapy, rubber band ligation) treatment fails, (2) concomitant symptomatic hemorrhoidal disease exists with other benign anorectal conditions (e.g., fistulas, fissures) that require surgery, (3) this is the patient's preference after surgical consultation, or (4) third-degree and fourth-degree hemorrhoids exist with severe signs and symptoms.

ANAL FISSURE

One of the most common causes of anorectal pain is anal fissure.6 Fissures occur in all age groups, most commonly in 30- to 50-year-olds. Men and women have equal prevalence.3z,58

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Etiology and Pathophysiology The majority of anal fissures are idiopathic. Possible causes include traumatic injury to the anal canal (such as with passage of a hard stool or severe diarrhea), infection, and hypertension of the anal sphincter.42, 52, 58 An anal fissure is a linear crack or slit (also referred commonly in the literature as an ulcer) in the squamous epithelium of the lower half of the anal canal, usually extending from below the dentate line to the anal verge.26,52, 74 Because of sensory innervation to this area, the fissure is painful. The fissure can be superficial or extend into the internal sphincter.74The fissure can become chronic and can be accompanied by other secondary changes such as a sentinel skin tag (located inferior to the fissure at the anal verge), hypertrophied anal papilla, or relative anal stenosis owing to spasm or a fibrotic internal sphincter (Fig. 3).23,52 In both sexes, the majority of fissures occur in the posterior midline wall of the anal cana1,52,58 the next most prevalent site being the anterior midline, where it is more common in women than in men. If a fissure is

Figure 3. Classic anal fissure composed of the following: hypertrophied anal papilla (A), fissure with exposed internal spinchter in base (B), and sentinel edematous skin tag (C). (From Fry RD, Kodner IJ: Anorectal disorders. In Erdelyi-Brown M (ed): Clinical Symposia. West Caldwell, NJ, Ciba Geigy 37:1,1985; with permission.)

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present in other locations it should be considered atypical, and other causes (e.g., Crohn’s disease, infections) should be investigated.l3.52, 55

Clinical Presentation and Diagnosis

Patients present with the main complaint of pain, especially with and following defecation. Patients may report avoidance of a bowel movement secondary to pain. The pain appears out of proportion to the size and seriousness of the lesion, and the patient can appear very reluctant to undergo examination. Hematochezia can occur but is usually minimal. Other less common symptoms include pruritus and mucous dis~harge.32.52~73~74 Physical examination of the anal canal can be difficult secondary to the patient’s pain. Visual inspection of the lower anal canal for a fissure (most commonly located in the posterior midline) can be done by spreading the patient’s buttocks and gently everting the anal verge. If a fissure is more chronic, a sentinel skin tag at the anal verge may give a clue to the presence of a fissure and its location, but should be differenti73 ated from a thrombosed external hemorrhoid or perianal Digital examination of the anal canal and anoscopy may be attempted, and pretreatment with lidocaine ointment may facilitate the examination. If digital examination or anoscopy cannot be performed, but a fissure can be observed by inspection, these procedures can be performed following initial treatment when the patient is in less pain.52, 73 However, if the diagnosis cannot be established it may be necessary to administer conscious sedation (e.g., midazolam) or possibly regional or general anesthesia to obtain the examination. If the fissure location is other than in the midline of the anal canal or multiple fissures are present, the lesion should be considered atypical. Specific underlying disease states should be sought including inflammatory bowel disease, leukemia, tuberculosis, chlamydia, gonorrhea, herpes, syphilis, carcinoma, and immunodeficiency syndromes.52, 55, 74

Treatment

Most anal fissures respond to a nonsurgical approach.23, 26 Treatment is aimed at pain control and healing of the fissure by promoting a regular soft stool and reducing the hypertonia and spasm of the internal rectal sphincter. Chronic anal fissures with secondary changes (e.g., setinel skin tag) are commonly refractory to conservative management.26 Medical management is used initially for treatment of an anal fissure. This includes a high-fiber diet, bulk laxatives, warm sitz baths

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(thought to decrease sphincter spasm), stool softener, topical anesthetics, and oral analgesics. Follow-up care should be with a primary care physician or specialist depending on the severity/chronicity of the fissure.52,73,74 The most commonly used surgical technique for the treatment of chronic fissures not responding to conservative treatment is lateral internal sphincterotomy (using either a subcutaneous or open approach)?', s*, s? The method is relatively simple, can be performed under local anesthesia in an outpatient setting, and has a high rate of fissure healing. Morbidity is minimal but can include abscess/fistula formation, postoperative hemorrhage, urinary retention, and incontinence to flatus or feces. Other surgical approaches include posterior internal sphincterotomy and manual anal dilation.74 Two types of pharmacologic treatment (nitroglycerin ointment and botulinum toxin) aimed at decreasing internal sphincter tone have been recently reported in the literature. G ~ r f i n examined e~~ the application of nitroglycerin ointment to the external anus and distal anal canal in a small number of patients with predominately acute superficial anal fissures. The majority of patients had prompt relief of pain and a high frequency of healing. JosP and Gui and associates3"induced reversible paralysis of the internal sphincter by injection of botulinum toxin (which inhibits acetylcholine release) in a small number of patients with chronic anal fissure. In both studies, the majority of patients had successful healing of fissures, and the treatment was well tolerated without major side effects. These two pharmacologic approaches appear promising; however, only a small number of patients have been studied to date. ANORECTALABSCESS

Anorectal abscesses are more common in men than women (2-3 : 1 ratio), and more than 50% of the abscesses occur in the 20- to 40-year age range. The highest incidence is noted in the spring and surnmer.'O, 44, The majority of anorectal abscesses are considered nonspecific or idiopathic?' The more frequent specific causes or predisposing factors associated with the development of anorectal abscesses include malignancy (especially hematologic malignancies), immunocompromised host, tuberculosis, actinomycosis, Crohn's disease, anal fissure, foreign body, and anorectal trauma.'O, 51, 70 Etiology and Pathophysiology

One of the more accepted pathogenic mechanisms for the formation of an anorectal abscess is the cryptoglandular theory.'", 21, 7" Anal glands

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(approximately 6 to 8) are located in the intersphincteric space (between the internal and external sphincters) circumferentially around the anal canal and drain into the anal crypts (at the level of the dentate line) via ducts that penetrate the internal sphincter. It is belived that the anal gland becomes infected and that the infection spreads to various abscess sites (Figs. 1 and 4). This theory, however, may not explain the causation of all idiopathic abscesses because evidence for infection of the anal gland was not observed in some patients with anorectal abscesses.” Mixed aerobic-anaerobic organisms are most frequently cultured from anorectal abscesses. Commonly found organisms are aerobes including Esckerickia coli, Proteus vulgaris, Staphylococcus aureus, and Streptococcus species and anaerobes including Bacteroides and Peptostreptococcus SP4, 51 Anorectal abscesses can be categorized based on anatomic location: perianal, ischiorectal, intersphincteric, and supralevator (above the levator ani) (see Fig. 4). The most common type of anorectal abscess is perianal (40% to 50%) and the least frequent is supralevator (2% to 90/0).10, 66, 67

Anal fistulas are believed to be the chronic form of an initial acute

Anal crypt

Supralevator space

levator ani

Figure 4. Perirectal abscesses. (From Marcus RH, Stine RJ, Cohen MA: Perirectal abscess. Ann Emerg Med 25:597, 1995; with permission.)

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anorectal abscess, but not all abscesses develop fistulas.10,23, 70 The incidence of fistula formation ranges from 25% to 50% if all four types of 67 abscesses are included.h6, By knowing the location of the external opening of the fistula, the internal opening of the fistula can be approximated using Goodsall's rule.21,69, 70 The rule is based on an imaginary transverse line drawn across the anus and states: if the external opening of the fistula is anterior to the transverse line, the internal opening will be a short, straight tract to the anal canal; if the external opening is posterior to the transverse line the tract will follow a curved course and open in the posterior midline of the anal 70

Clinical Presentation and Diagnosis Pain is the most common presenting complaint of all four types of abscesses. The exact type of the abscess will determine the location and character of the pain. Perianal abscesses are most easy to recognize because they are superficial and present with a palpable, painful mass in the perianal area near the anal verge. Patients complain of a localized area of throbbing perianal pain that is exacerbated by sitting, coughing, or defecation. Fever and leukocytosis are uncommon.10,23 An ischiorectal abscess can produce pain that is felt in the buttock although few external signs are present, or it can also present as a large, indurated, erythematous, tender mass of the buttock area. Fever is more common than in perianal abscess. Digital examination of the anorectum may reveal an area of induration and tenderness above the dentate line, and bidigital examination may reveal an area of induration of the perianal/buttock area.l"*l3 Intersphincteric abscesses are associated with pain in the anal canal and rectum, which is exacerbated by defecation; a mucous or exudative rectal discharge may be noted; and fever may be present. Digital examination may reveal a tender mass of the anal canal or distal recturn.'O, With supralevator abscesses, patients present with either buttock or perianal pain and no external findings (unless extension to another tissue space has occurred); fever and leukocytosis is common, and urinary retention may also be present.25,63 A case of a patient presenting with low back pain and sciatica with a final diagnosis of supralevator abscess has also been reported.33Digital examination may reveal a tender mass in the upper anal canal/distal rectum. Needle aspiration may be needed to confirm a diagnosis of abscess.'" Digital examination, anoscopy, or sigmoidoscopy may all need to be performed to determine a definitive diagnosis. These procedures may

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require regional or general anesthesia secondary to the patient’s pain or sphincter spasm.51Nitrous oxide administration to the patient in the emergency department may enable a more complete e~amination.’~

Treatment and Disposition Definitive treatment for an anorectal abscess is timely surgical incision and drainage. If the abscess is not drained promptly, it can cause needless pain, extend into other adjacent spaces, and produce serious infection.10,23, 35, 51 Even if the examination does not reveal palpable fluctuance or induration, ”the presence of pain suggests the need to drain” (attributed to I. J. Kodner, by Cormanlo).The painful or erythematous area can be examined for pus by needle aspiration to confirm the diagnosis, and then incision and drainage can be performed.1° In the emergency department it is recommended that only patients with small, superficial abscesses undergo incision and drainage under local anesthesia; the vast majority of these abscesses will be of the perianal variety.13,23, 51, These recommendations are based on the observation that for larger and more complicated abscesses, adequate drainage of the abscess and proper anorectum examination cannot be performed well under local anesthesia.81 It is difficult to achieve complete anesthesia of the abscess cavity using local anesthetics because of the thin skin covering the abscess, decreased anesthetic activity at low pH found in infected areas, and further distention of the cavity with associated increased pain with infiltration of anesthetic. A suggested technique is to inject the dome of the abscess subcutaneously with local anesthetic using a 25-gauge needle to spread anesthesia through the subcutaneous layers into the surrounding skin. An alternate approach is to infiltrate intradermally around the periphery of the 81 Narcotic analgesics, conscious sedation with benzodiazepines, or administration of nitrous oxide may also be used to provide adequate ana1ge~ia.l~. 81 Following anesthesia, an incision is made into the anorectal abscess as close to the anal verge as possible to avoid formation of a long fistulous tract.’O, The pus is drained and loculations are evacuated by blunt dissection. Culturing the pus is usually not performed because antibiotics are infrequently used. Some authors have shown, however, that the likelihood of a fistula is much greater in the presence of gutderived organisms (E. coli, Bacteroides fiagilis), and recommend culture and a re-examination for fistula only if gut-derived organisms are cultured.17,28 Following incision and drainage, the abscess cavity is packed with iodoform gauze. The patient should be instructed to remove the packing

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in 24 hours and to start sitz baths 2 to 3 times a day. An analgesic should be prescribed. The patient should return to the emergency department if pain is not improved over the next 48 hours or if signs or symptoms of worsening infection develop. Surgical referral of the patient is needed for follow-up inspection of the wound in 24 to 48 hours and for followup evaluation for development of a fistula. Antibiotics are not needed following drainage, unless marked cellulitis, immunosuppression, valvular heart disease, signs of systemic infection, or diabetes exists,'Q13, 51 and in most of these cases inpatient care with systemic antibiotics would be prudent. Patients with ischiorectal abscesses can undergo incision and drainage as an outpatient using local anesthetic; however, if the patient is febrile, inpatient hospitalization with administration of systemic antibiotics is recommended.10 Both interspinchteric and supralevator abscesses need to be drained in the operating suite under regional or general anesthesia. Definitive treatment of an intersphincteric abscess requires excision of the abscess via an internal sphinchterotomy.l0Z21 Depending on the exact location and extent of a supralevator abscess, surgical drainage may be via the rectum, perineum, or the vagina.lfl,25, 63

MALIGNANT ANAL TUMORS

Anal tumors (tumors of the anal canal and anal margin) are relatively rare, accounting for only 1%to 6% of all anorectal t ~ r n 0 r s . The l~ incidence of anal cancer increases with age, with an approximate mean age range at presentation of 60 to 70 years old. Anal canal tumors are predominant in females (2 : 1 to 5 : 1, fema1e:male ratios), and anal margin tumors are more frequently found in males (approximate ma1e:female ratio of 4 : l).l4,59 There continues to be confusion in the literature in the anatomic designation of the area of the anal margin in reference to anal carcinom a ~ .For ' ~ example, some authors define any tumor occurring below the dentate line as originating in the anal and others consider the anal margin distal to the anal verge.59

Etiology and Pathophysiology

A number of environmental risk factors have been associated with a higher incidence of anal cancer including cigarette smoking, anal intercourse, and radiation exposure. The human papilloma virus (HPV) has also been associated with anal cancer, HPV type 16 being the major

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virus linked with epidermoid or squamous cell anal carcinoma. A higher incidence of anal cancer is also found in patients with Crohn’s disease. Immunosuppressed patients are also at higher risk for anal carcinoma as shown in renal transplant patientP and patients with AIDS.54Anal cancers in immunosuppressed patients are more likely associated with HPV, occur at a younger age, and progress ra~id1y.I~ The anal canal, which extends from the anorectal ring to the anal verge, has a diversity of cell types. Below the dentate line, the anal canal is lined with squamous epithelial cells, which lack glands. Distal to the anal verge the squamous epithelium becomes keratinized and contains eccrine and apocrine glands and also hair follicle^.^^ Proximal to the dentate line (at the union of embryonic ectoderm and endoderm), a transitional zone exists where the cell type changes from squamous epithelium to columnar epithelium. This transitional zone contains transitional cells, squamous cells, columnar cells, endocrine cells, melanocytes, and anal glandular cells. At the cephaled end of the transitional zone, rectal columnar epithelium predominate^.^^ Because of the diverse histology of the anal region, many different types of malignancies can develop. The most prevalent (80% to 95%) types of anal cancer, however, both at the anal margin and canal are the squamous cell or epidermoid carcinomas (which includes basaloid and mucoepidermoid carcinomas found at the anal transitional zone).2,14, 5y, 64 Other types of carcinoma are relatively rare. In the anal margin, they include melanoma, basal cell carcinoma, Bowen’s disease, and Paget’s disease. In the anal canal, they include adenocarcinoma, melanoma, and endocrine cancer^.'^, 59, 64 Anal canal tumors are characteristically infiltrative and not polypoid masses, and lower canal lesions tend to develop infiltrating ulcers.,Anal canal tumors usually only involve part of the canal, whereas anal margin lesions tend to be ~ircumferential.’~

Clinical Presentation and Diagnosis

Patient symptoms are usually nonspecific, and the three most frequent symptoms are rectal bleeding (most common), anal pain, and sensation of a rectal mass.l, 64 Other symptoms include constipation, diarrhea, discharge, and pruritis. In one review of 109 patients presenting for evaluation of anal itching, 6% had an anal cancer.” The above nonspecific symptoms are also associated with many benign anorectal disorders, and therefore it is obvious that initial patient workup and subsequent follow-up in patients presenting with anorectal complaints should include differentiation of these benign disorders from malignant ones. In one studyI6of 22 patients treated for anal carcinoma,

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the majority (76%) of tumors were initially incorrectly diagnosed as benign anorectal disorders by the referring physician, thus delaying start of treatment. Therefore, a high index of suspicion and thorough evaluations are important when evaluating anorectal complaints. The main role of the emergency physician concerning malignant anal tumors is to recognize or suspect their presence on physical examination (with the help of the clinical history) and to facilitate an appropriate surgical evaluation for possible diagnostic biopsy. In the emergency department's evaluation of anorectal complaints, a workup is not complete until digital examination and anoscopy are performed. Referral to other specialists may also be necessary for further diagnostic investigations (e.g., sigmoidoscopy, colonoscopy). On physical examination if any suspicious anorectal mass (most commonly an infiltrating lesion) or chronic ulceration is detected by inspection, palpation, or anoscopy, surgical referral should be obtained. Chronic anorectal complaints or pigment change of the anal region also should be considered suspicious for malignancy.sy Rectal bleeding should be thoroughly investigated and an exact diagnosis determined. Treatment and Disposition

Although treatment of anal carcinomas is referred to other specialists, the emergency physician should have a general appreciation of treatment modalities. Treatment of anal carcinomas depends on the cell type, whether the carcinoma is at the anal margin or located in the anal canal, the size of the tumor, and spread of the lesion.59 Local surgical excision of both anal margin (with superficial or microinvasive disease) and anal canal (lesions less than 2 cm and not involving the dentate line) squamous cell tumors has an excellent 5-year survival rate.2,14, 59, 64 Less than 10% of patients that present with anal canal tumors, however, are suitable for local excision compared with greater than 60% with anal margin tumors. Reasons for this discrepancy include late patient presentation for eval~ation,5~ delayed physician diagnosis (secondary to misdiagnosis of other common anorectal disorders),16and the greater propensity for anal canal tumors to become invasive and metastasize compared with anal margin tumors.1 Anal margin tumors that are more invasive, with anal sphincter involvement or metastasis to the inguinal lymph nodes, have been effectively treated with radiotherapy and combined radiotherapy and chemotherapy, with or without surgery (local excision or abdominoperineal re~ection).'~, 59 The majority of anal canal tumors were historically all treated with abdominoperineal resection until the late 1 9 7 0 ~ when ~ radiotherapy was

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shown to have a role. In the 1980s, good results were obtained with combined radiotherapy and ~hemotherapy.~~ In the 1990s, the 5-year survival for combined chemotherapy (5-FU and mitomycin C) and radiotherapy (external beam radiation) is similar to or better than abdominoperineal rese~ti0n.I~ The combined therapy approach has a 5-year survival of 60% to 80% and 80% preservation of anal function. It has now become the treatment of choice by many centers, and abdominoperineal resection is used as a salvage procedure in patients with local recurrence or who have destruction of the sphincter.14

INFECTIONS OF THE ANORECTUM

It has been reported that between 4% and 13% of the adult male population of the United States is homosexual or bisexual for a significant portion of their lives. Promiscuity is common in the homosexual p o p ~ l a t i o n .82~ ~Sexually , transmitted diseases of the colon, anus, and rectum have been referred to as the ”gay bowel syndrome.”” It is known, however, that sexual promiscuity and the practice of receptive anal intercourse are the factors involved in contracting anorectal sexually transmitted infections. Therefore, women who practice receptive anal intercourse are also at risk for sexually transmitted diseases of the anorectum.s6Monogamous homosexuals have no greater risk of sexually transmitted diseases than monogamous heterosexuals.

Bacterial Infections

Chlamydial Infections

Anogenital chlamydia1infection is the most common sexually transmitted disease in the United States,79with an estimated 3 million infections annually? Fifteen immunotypes are known to exist, with serotypes D and K responsible for proctitis and serotypes L1, L2, and L, responsible for lymphogranuloma venereum (LGV).Chlamydial infections are transmitted to the anorectum via anorectal or oral-anal interc~urse.~~, 82 Up to 15% of infected individuals are asymptomatic. Patients with non-LGV infections may present with rectal pain, tenesmus, and fever. Sigmoidoscopic examination reveals nonspecific proctitis with mucosal erythema. Occasionally mucosal ulcerations are seen. Inguinal lymphadenopathy may be present. LGV disease presents with pain and tenesmus as well. The sigmoidoscopic findings reveal a more severe proctitis similar to Crohn’s proctitis. The mucosa is erythematous, friable, and

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ulcerated. The lymphadenopathy is more pronounced, and the inguinal nodes may be matted. Untreated LGV may result in rectovaginal or rectovesical fistulae, abscesses, and rectal stricture^.^^ The diagnosis should be confirmed by biopsy and tissue culture. Treatment options include doxycycline 100 mg orally twice daily for 7 days or azithromycin 1 g orally as a single dose or ofloxacin 300 mg orally twice daily for 7 days.79Treatment for LGV should be continued for 21 days.", 82 Erythromycin base 500 mg orally four times a day for 7 days may be used in the pregnant patient. Sexual contacts of infected people should be treated.

Gonorrhea Gonorrhea is caused by an intracellular gram-negative diplococci, Neisseriu gonovrhoeae. Anorectal infection has been reported in 45Y0~~ to of homosexual males and in 45% of women with uncomplicated gonorrhea. Lone rectal involvement occurs in 4%43and 6%56,82 of women. Gonorrhea is mostly transmitted through anal intercourse in men. In women, gonorrhea is commonly transmitted to the anorectum by autoinoculation from the vagina.8z The incubation period is 5 to 7 days. The majority of infected individuals are asymptomatic with only about 10% of infected patients displaying When symptoms do occur, patients experience tenesmus, pruritis, and a bloody or mucoid anal discharge. Disseminated disease can occur, resulting in perihepatitis, meningitis, arthritis, endocarditis, and pericarditi~.~~. 82 Anoscopy reveals an erythematous, friable rectal mucosa with superficial erosions and a mucopurulent, bloody discharge.43The ability to express pus from anal crypts is highly suggestive of gonorrhea. The diagnosis can be suggested by the examination and confirmed by a positive Gram stain of the mucopurulent discharge or a positive culture grown on Thayer-Martin media. Empiric therapy should begin with suspicion of the disease. Recommended treatment protocols for uncomplicated infections include a single dose of ceftriaxone 125 mg intramuscularly or cefixime 400 mg orally or ciprofloxacin 500 mg orally or ofloxacin 400 mg orally.79Because of the high rate of coinfection with Chlumydia fruchornutis, it is recommended that the patient be treated with doxycycline 100 mg twice daily for 7 days. All sexual partners should be treated.

Chancroid Chancroid is caused by Hemophilus ducveyi, and accounts for up to 5% of anogenital ulcer disease in the United States. The disease is

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manifested by tender anorectal or genital ulcers, painful lymphadenopathy, and perianal abscesses. Lymphadenopathy is present in about half of the cases. The diagnosis is confirmed by culture.56Treatment options for chancroid include ceftriaxone 250 mg intramuscularly as a single dose or azithromycin 1 g orally in a single dose or erythromycin base 500 mg orally four times daily for 7 days.7y Shigella

Shigellosis is caused by Shigeflaj7exneri. Between 30% and 50% of cases of shigellosis in New York City, San Francisco, and Seattle occur in the homosexual population.R2The bacterium is transmitted by direct or indirect fecal-to-oral transmission. The infected patient will present with abdominal cramping, nausea, fever, and bloody diarrhea. The diarrhea may result in dehydration. The mucosa will appear friable and hyperemic with ulcerations on sigmoidoscopic examination. The diagnosis should be suspected because of the presentation and the presence of fecal leukocytes. The diagnosis is confirmed by stool culture. Acute treatment of shigellosis includes intravenous hydration and antibiotics. Antibiotic options include ciprofloxacin 500 mg twice daily for 7 days or double strength trimethoprim-sulfamethoxazole one tablet twice daily for 7 days.

Viral Infections Herpes Simplex Virus

Herpes simplex virus type 2 (HSV2) accounts for approximately 90% of anorectal herpes infections. Serologic tests indicate that more than 95% of male homosexual patients have been infected with HSV2.56 Ulcerative perianal HSV2 lesions that are present for 1 month or more with no other cause of immunodeficiency in a patient with laboratory evidence of HIV infection is diagnostic of AIDS.s2 Perianal HSV infections are transmitted through anorectal intercourse. Symptoms appear 4 to 21 days after initial inoculation. The patient will experience rectal pain, tenesmus, mucopurulent discharge, and constipation. Fecal impaction may result from the severe pain associated with defecation. Pruritis ani can be seen in up to 85% of patients infected with HSV2.82Systemic symptoms of fever, chills, and malaise may occur. Bilateral inguinal lymphadenopathy may be present. The patient may also experience sacral parasthesia, pain radiating down the posterior thighs, impotence, and urinary retention owing to autonomic nervous system involvement.8The pain associated with the acute infec-

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tion may require topical anesthetics to allow for proper examination. Proctoscopy will reveal a friable, ulcerated rectal mucosa in the distal 10 cm of the rectum, associated with a mucopurulent discharge. Symptoms of the initial infection last for 7 to 10 days. Approximately 80% of patients experiencing the first episode of HSV2 infection will experience a recurrence in 1 year. Recurrent infections are usually mild and not associated with systemic symptoms. The diagnosis can be confirmed by viral culture. Treatment includes analgesics, stool softeners, and antiviral agents. Oral acyclovir 200 mg to 400 mg five times daily for 10 days will reduce the length of pain and viral shedding and enhance healing. Topical acyclovir has not been as effective as oral acyclovir in treating anorectal HSV infections. Some authors recommend the concomitant use of topical and oral acyclovir.82 Intravenous acyclovir can be used in severe cases of HSV infection. Acyclovir-resistant HSV has been documented, although more commonly in HIV-positive patients.56 Condylomata A cuminata

Human papillomavirus (HPV) causes warts in many locations including the anorectum. HPV types 6, 11, 16, and 18 are most commonly associated with perianal condylomata. Types 16 and 18 have been associated with anal dysplasia, intraepithelial neoplasia, and invasive squamous cell car~inoma.~, 50 The majority of patients with anal condylomata are homosexual. It has been estimated that 50% to 75% of asymptomatic homosexuals may harbor anal condylomata.s6HPV is most commonly spread to the anorectum via anal receptive intercourse; however, close nonsexual contact may also allow for transmission. After inoculation there is an incubation period of 1 to 6 months. The patient will present with lesions appearing rough and cauliflowerlike with fingerlike projections. Patients may also complain of pruritus ani, bleeding, discharge, and pain. In 84% of patients with condyloma accuminata, perianal and intra-anal lesions are present. In 10% of patients, only intra-anal lesions are present. Therefore, anoscopy is mandatory because treatment of perianal lesions will be unsuccessful if intraanal lesions are not treated concomitantly.s6The diagnosis is made by the appearance of the lesions, although condyloma lata and squamous cell carcinoma should be considered. The diagnosis can be confirmed by biopsy if uncertain. Multiple treatment options are available for condylomata accuminata. Chemical treatment with podophyllin, a cytotoxic resin, has been used for many years. Because of its irritating effects it should not be applied to intra-anal lesion^.^" Trichloroacetic acid can be applied to the perianal region and in the anal canal. Both podophyllin and trichloroace-

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tic acid require multiple applications applied weekly. Cryotherapy using liquid nitrogen or nitrous oxide has also been used successfully to treat perianal condyloma. This therapy is also done weekly until the warts resolve. Other methods of physical removal include surgical excision, electrocoagulation therapy, and laser removal with a carbon dioxide laser. Immunotherapy with an autologous vaccine or interferon has also been used to treat condylomata acc~minata.~, 50,56 It has been shown that HPV DNA is found in warts, white areas of skin after application of acetic acid, and in clinically normal skin in the perianal regi0n.3~This may explain the high recurrence rate of HPV. No treatment has been shown to totally eradicate the human papilloma virus.5o

Spirochetes

Syphilis

Primary anal syphilis is caused by the spirochete Tveponema pallidum and is most commonly seen in homosexual males. The disease is spread through anoreceptive intercourse. The incubation period is usually 2 to 6 weeks but can be up to 6 months. Primary syphilis manifests as an irregular, eccentrically located ulcer (chancre) that classically is painless. The ulcer may be very painful, however, and may be misdiagnosed as an anal fissure. The lesions may be multiple, and may occur opposite each other in a ”mirror image” or ”kissing” config~ration.~~, 82 Inguinal adenopathy may be present and may be mistaken for lymphoma. If untreated, the lesions will resolve spontaneously in 3 to 4 weeks. Two to 10 weeks later a diffuse maculopapular rash will develop, commonly involving the palms of the hands and soles of the feet. This manifestation of secondary syphilis may be accompanied by a perianal, pale brown or pink flat verucous lesion. This perianal mass is usually pruritic, malodorous, and mucus secreting. The lesion is condyloma latum and must be differentiated from condylomata accuminata, because the lesion is infective. The differentiation can be made by demonstrating the spirochete on darkfield microscopy. Untreated secondary syphilis may progress to late or latent syphilis, which occurs more than 1 year after the initial infection. This can affect the central nervous system, cardiovascular system, particularly the aorta, and also the kidneys and liver. Syphilitic rectal gummas occur very rarely.56,** The diagnosis of primary syphilis is made by identifying the spirochete with darkfield microscopy and a reactive fluorescent treponemal antibody (FTA) absorption test. The FTA becomes positive 4 to 6 weeks after initial infection, before the Venereal Disease Research Laboratories or rapid plasma ~ e a g i nThe . ~ ~treatment of primary and secondary syphi-

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lis and latent syphilis of less than 1 year’s duration is benzathine penicillin G, 2.4 million units intramuscularly as a single dose. The treatment of latent syphilis of more than 1 year’s duration or of unknown duration is benzathine penicillin G, 2.4 million units intramuscularly, weekly for three consecutive weeks.79It is recommended that patients infected with HIV be treated with the regimen used for latent syphilis. Erythromycin or tetracycline, 500 mg four times a day for 15 days, can be used in penicillin-allergic patients.56All sexual contacts of an infected individual over the past 12 months should be treated.

Parasites

Amebiasis

Entamoeba histolytica is a protozoan that exists in the colon as either a trophozoite or a cyst. The prevalence of E. histolytica in homosexual and bisexual men is 20% to 32%. Transmission occurs through oral-anal intercourse. Infected patients may be asymptomatic or may experience abdominal pain, bloody diarrhea, fever, tenesmus, and malaise. Sigmoidoscopy may reveal a friable, erythematous mucosa with ”hourglass”appearing ulcers. The diagnosis is made by stool examination for ova and parasites. Treatment for mild to moderate infection is metronidazole 750 mg three times daily for 10 days. For patients with severe infections, oral diiodohydroxyquin 650 mg three times daily for 3 weeks is given following the metronidazole therapy.82 Giardiasis The causative organism of giardiasis is Giardia Zamblia. The incidence in the homosexual population is between 4% and 18%. It is transmitted through oral-anal intercourse. The patient may present with abdominal cramping, anorexia, and weight loss. The patient will also complain of foul-smelling, frequent, loose stools. The diagnosis is made by stool examination for ova and parasites. If the stools are not diagnostic and the diagnosis is suspected, a duodenal aspirate or small bowel biopsy can be done. The treatment consists of metronidazole 250 mg three times daily for 7 days.82

Anorectal Manifestations of HIV

Infection with a sexually transmitted disease increases the number of reactive leukocytes that are susceptible to HIV infection. The number

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of leukocytes in the semen and vaginal secretions is higher in patients infected with sexually transmitted diseases. This increases the likelihood of HIV transmission in patients with other sexually transmitted dise a s e ~ Homosexual .~~ men with rectal spirochaetosis were four times more likely to be infected with HIV than those with no evidence of rectal spirochaetosis in their biopsy Coinfection with HIV may alter the severity and manifestations of other sexually transmitted diseases. Syphilis may present atypically, with false-positive or false-negative serologic tests. It may progress more rapidly to involve the central nervous system, and treatment failure is more common. Treatment with benzathine penicillin G, 2.4 million units weekly for 3 consecutive weeks should be considered. HSV2 infections are more severe and recurrences are more frequent. Suppressive therapy with acyclovir 400 mg three to four times daily is recommended. Acyclovir-resistant strains of HSV2 are more common in HIV-infected patients Foscarnet has been used successfully in this situation. The incidence of chancroid is increased in HIV-infected patients. The ulcers are larger and more persistent. Treatment failures are six times more common. HPV infection in HIV patients is more aggressive with a greater propensity for dysplastic and neoplastic changes.56 Other anorectal manifestations of HIV include opportunistic infections resulting in diarrheal disease. These include cytomegalovirus, cryptosporidiosis, and mycobacterium avium-intracellulare. They can result in dehydration and gastrointestinal hemorrhage and generally do not respond well to medical therapy.56, Nonspecific proctitis with no identifiable pathogenic agent has been noted in 26% of patients infected with HIV.4sMalignancies including Kaposi’s sarcoma, lymphoma, and squamous cell carcinoma can present with anorectal symptoms in the patient infected with HIV. Benign anal fissures, anal ulcerations, hemorrhoids, and perianal sepsis are common problems of the HIV-infected patient.56,6 0 , 8 2

RECTAL TRAUMA

Anorectal injuries are relatively uncommon in the civilian population.36 Penetrating rectal trauma is the most common noniatrogenic mechanism of anorectal trauma. Other mechanisms include blunt pelvic or perineal trauma, iatrogenic injuries, injuries related to foreign bodies, and injuries secondary to parturition.

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Etiology Penetrating Trauma

The most common noniatrogenic cause of anorectal trauma is gunshot wounds to the buttocks and perineum.22Stab wounds from a knife or other sharp instrument, impalement or injury owing to sexual assault may also result in anorectal injury. Most civilian gunshot wounds are caused by low-velocity weapons (
Rectal injury caused by blunt trauma is uncommon, occurring in 2.2%12 to 5%36,7h of cases. Blunt abdominal and pelvic trauma resulting from motor vehicle accidents is most common. Other mechanisms include crush injuries and jet enemas. A case was reported of a middleaged woman who fell on her sacrum and back while water skiing at 60 rniles/hour resulting in a jet enema. The high-pressure water enema resulted in a full thickness rectal tear and an extensive pelvic and retroperitoneal h e r n a t ~ m a .Although ~~ rectal injuries caused by blunt trauma are rare, they may lead to pelvic abscess formation, sepsis, and an increase in morbidity and mortality. Most morbidity and mortality from blunt pelvoperineal injuries are related to concurrent head and torso injuries12; however, late septic mortality from blunt peIviperinea1 injuries reaches 18% to 25y0.l~ Iatrogenic Trauma

The most common cause of anorectal trauma is iatrogenic.21Perforation of the bowel occurs in up to 0.04% of patients who have a barium enema. This is the most common complication of this p r o c e d ~ r eMost .~~ perforations are related to underlying disease or trauma reducing the strength of the bowel wall. Potential mechanisms include inflammatory bowel disease, neoplasm, diverticulitis, and bowel ischemia. Local trauma from the enema tip, retention balloon, or previous mucosal biopsy will also increase the risk of perforation.x3Trauma from the enema tip or retention balloon is the most common cause of perforation during a barium enema. Rectal perforation may also occur owing to excessive hydrostatic pressure during the infusion of the barium.31Extravasated barium results in a chemical peritonitis that causes a hypoten-

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sive state that can be fatal if not treated aggre~sively,~~ with mortality approaching 50y0.~~ There is a 0.2% perforation rate for diagnostic colonoscopy and 0.29% to 0.42% perforation rate during p o l y p e c t ~ m yHemorrhage .~~ may also complicate colonoscopy, occurring in 1% of patients.78 A bowel perforation sustained during a colonoscopy may respond to conservative management because the perforations are usually small and the bowel was prepared similarly to the preparation used for a colon resection. Surgical procedures including hemorrhoidectomy, anal fistulotomy, and anal sphincterotomy may lead to anorectal injury resulting in infection, incontinence, anal stricture, and ectropian.22Gynecologic procedures such as uterine dilatation and curettage and hysterectomy may lead to rectal perforation with subsequent infection or rectovaginal fistulas. Rectal perforation of a migrating intrauterine device has also been reported. Urologic procedures including radial cycstectomy, suprapubic, and perineal prostatectomy and transurethral resection of the prostate have been complicated by rectal injury. Vaginal deliveries may also result in injury to the anus or rectum. Macrosomia, shoulder dystocia, and forceps delivery may result in an anal sphincter tear. It is uncertain whether an episiotomy will prevent anorectal trauma during delivery.22 Rectal thermometers and therapeutic enemas are also a source of rectal injury and perforation. Most perforations due to therapeutic enemas occur along the anterior rectal wall. The perforations may be extraperitoneal or intraperitoneal and may result in abscess formation, sepsis, hemorrhage, and fistula formation.22 Foreign Bodies Rectal foreign bodies may be inserted or the result of ingested foreign bodies such as toothpicks, chicken bones, fish bones, or sunflower seeds. The ingested foreign body may be difficult to diagnose if a history of ingested foreign body is not obtained or if the patient is unaware of the ingestion. The presentation may be similar to that of a perirectal abscess; however, the foreign body will most often be revealed by adequate rectal examinationF2Foreign bodies inserted during autoerotic or homosexual practices may lead to retained foreign bodies, nontransmural rectal lacerations, anal sphincter injury, and perforation above or below the peritoneal refle~tion.~~ Pathophysiology

Although the cause of anorectal injury and time since injury are important in determining the possible complications and treatment, the

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location of injury is also important. Isolated anal trauma is rare and most commonly a result of obstetric causes. Injuries below the peritoneal reflection are more likely to result in retroperitoneal injuries and, depending on their depth, may be amenable to conservative therapy. Injuries above the peritoneal reflection result in intraperitoneal perforation and contamination, almost always necessitating laparotomy, debridement of devitalized tissue, sacral drainage, and possible colostomy.22

Clinical Presentation History

If the patient is able to provide a history of the event, it is important to determine the cause of the injury, penetrating or blunt, whether the patient has had a recent transrectal diagnostic or therapeutic procedure, the timing of the injury, and presenting symptoms. The most common presenting symptoms include abdominal, perineal or anal pain, blood per rectum, and fever. It is, of course, always necessary to obtain a medical history, surgical history, allergy and medication history; determine the tetanus status; and determine the time of the last meal. Physical Examination The examination of the pelvic structures should occur during the secondary survey of a trauma resuscitation. Only the focused examination related to the detection of anorectal trauma is discussed. The examination should begin with the inspection of the buttocks, perineum, and anus. Any evidence of penetrating injury, impalement, or tear of the integument should be noted. In blunt trauma, a rectal injury that accompanies a pelvic fracture can generally be detected by physical examination. The physical findings include a tear of the integument of the perineum or palpable rectal tear on rectal examination.80The thighs, buttocks, and abdomen should be palpated for the presence of tenderness, swelling, crepitance, or peritoneal signs. Crepitance may be a delayed sign of sepsis, occurring 24 to 48 hours after an unrecognized extraperitoneal perforation.22 A digital rectal examination should be performed on all patients even if no external sign of trauma is noted. It is important to note the position of the anus because blunt trauma may avulse the anus from its muscular attachments. The examiner should note the presence of gross or occult blood on rectal examination, the presence of palpable rectal defects, and the position of the prostate. In cases where external perineal

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injury is noted, the presence of occult blood in the stool may not be reliable owing to the presence of gross blood in the perineal region. Rectal examination has been shown to have positive findings (gross blood or palpable defect) in 75%19 to of patients. Because of the proximity of genitourinary structures to the anorectum, one should have a high suspicion for concurrent injury. The examiner should observe the presence of blood at the urethral meatus, abnormal prostrate position, scrota1 hematoma, and vaginal bleeding. A vaginal examination should be performed if there is any possibility of pelvic or perineal injury. The genitourinary tract is the most common secondary system injured in penetrating rectal trauma. Franko and associateszonoted 17 concurrent genitourinary injuries in 200 cases of penetrating rectal trauma over a 13year period. The concurrent genitourinary injuries included 13 bladder injuries, 3 urethral injuries, and 1 ureteral injury. Complications secondary to these injuries included pelvic, suprapubic and subphrenic abscesses, rectovesical and rectourethral fistulas, chronic urinary tract infections, urinary bladder stones, and urethral strictures.20 Management General

As with all trauma patients, the initial management of a patient with anorectal trauma includes the primary survey, resuscitation phase, secondary survey, and definitive care phase. During the primary survey the airway is controlled, the c-spine is stabilized, the breathing and ventilation are assessed, and life-saving measures are initiated. The circulatory and cardiac status and blood volume are assessed. Two largebore intravenous lines are established, and crystalloid, blood, and blood products are infused as required. Significant external hemorrhage is also controlled. During the resuscitation phase, the management of lifethreatening problems is continued, shock management is continued, and a nasogastric tube and a foley catheter are inserted, if not contraindicated. It is during the secondary survey that a complete head-to-toe examination is performed and anorectal injury should be noted. The management of anorectal injury is performed during the definitive care phase of the trauma resuscitation. Because of the presence of clostridium tetani in the feces, any patient with suspected anorectal injury should receive tetanus prophylaxis. Diagnostic Studies

Plain radiographic studies of the abdomen and pelvis can be helpful when evaluating a patient for potential anorectal trauma. Supine and

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upright abdominal radiographs may demonstrate extraluminal air from an intraperitoneal perforation or the location of a projectile.lYAnteroposterior and lateral pelvic films may reveal pelvic fractures or diasthesis of the symphysis pubis suggesting a potential rectal injury. Perirectal soft-tissue densities or extraluminal air may also be noted, indicating rectal perforation and hematoma formation.22 Proctosigmoidoscopy should be performed when evaluating a patient for potential anorectal trauma when the following occur: there is no other indication for laparotomy, rectal injury is suggested by the patient’s history, rectal injury is suggested by the supposed path of a bullet, blood is evident on rectal examination, or there is a high suspicion of rectal injury. Proctosigmoidoscopy is positive if there is evidence of gross blood or perforation.36Indications for laparotomy include physical examination consistent with an acute abdomen, radiographs revealing an intra-abdominal projectile or extraluminal air, evidence of a deep rectal perforation, or a defect on rectal examination or sigmoidoscopy.’9,22 Contrast enemas are rarely useful, but may be beneficial in unclear cases. If contrast enemas are used to determine the presence of colorectal perforation, water-soluble contrast media such as diatrizoate should be used to prevent the complications of extravasated barium.2z Management of Penetrating or Blunt Anorectal Trauma Rectal injuries confined to the mucosa may be treated by irrigation and primary repair or may not require treatment at all. Deep rectal injuries and perforations require debridement of devitalized tissue; primary repair if the perforation is easily identified; a diverting colostomy; and transperineal, presacral drainage.3,12, 36, 68 The use of distal rectal irrigation is uncertain; however, it is recommended when rectal injury is caused by blunt trauma,12 there is extensive soft-tissue injury? 36 the injury is caused by high-velocity military or there is evidence of a foreign body or bone fragments associated with the injury.3 Falcone and co-workers18have proposed the use of primary repair with intracolonic bypass as an alternative to a diverting colostomy. All patients undergoing laparotomy require broad-spectrum intravenous antibiotics. Potential antibiotics include cefoxitin, cefotetan, or a combination of ampicillin, gentamicin, and clindamycin.’*,36 Tetanus prophylaxis is mandatory when treating patients with rectal perforation. iatrogenic Trauma Rectal perforations sustained during a barium enema may be treated conservatively if the perforation is localized, extraperitoneal, and con-

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tains small amounts of extravasated barium. Conservative management includes broad-spectrum intravenous antibiotics and close observation. Extraperitoneal perforations with gross extravasation and intraperitoneal perforations require aggressive fluid resuscitation, intravenous antibiotics, and laparotomy. Surgical treatment includes irrigation and gentle debridement of the barium from the peritoneal surfaces and omentum and primary repair or resection of the perforation. If the extravasation is extensive, a diverting colostomy and presacral drainage may be warranted.22,31, 78 Proctosigmoidoscopy or colonoscopy may result in perforation of the rectum. Because the bowel perforations secondary to endoscopic procedures are usually small and the preparation for rectal and colonic procedures is similar to that used for bowel resections, conservative management has been used successfully to treat this complication. Nonoperative management includes intravenous fluids, intravenous broadspectrum antibiotics, nasogastric suction, and close observation. If the patient develops increasing abdominal tenderness, fever, tachycardia or other evidence of peritonitis, then surgical treatment is required.7R Disposition

A surgical consultation is suggested for patients sustaining rectal trauma. The patient with anorectal trauma will require admission for all but superficial rectal tears that are proved to be superficial by proctosigmoidoscopy.

SUMMARY

Anorectal disorders are commonly encountered in the practice of emergency medicine. Most can be diagnosed and treated in the emergency department setting. Almost all anorectal disorders once diagnosed and treated in the emergency department need appropriate follow-up to ensure adequacy of treatment, for further possible diagnostic procedures (e.g., endoscopy, biopsy), or for definitive treatment. Hemorrhoids are the most prevalent anorectal disorder and are the most common cause of hematochezia. Treatment is dependent on the degree of hemorrhoid prolapse and symptoms. Most cases can be treated by conservative medical treatment (e.g., dietary changes, sitz baths) or nonsurgical procedures (e.g., rubber band liagation, infrared coagulation). Surgical excision of symptomatic thrombosed external hemorrhoids is indicated if within 48 to 72 hours of pain onset. Anal fissures are one of the most common causes of anorectal pain. They are most frequently idiopathic, and most are located in the poste-

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rior midline of the anal canal. Most anal fissures are adequately treated by a medical approach using sitz baths, stool softeners, and analgesics. If the anal fissure becomes chronic and is not responsive to medical therapy, a lateral sphincterotomy of the internal anal sphincter is the surgical procedure of choice. Pharmacologic treatment (botulinum toxin or nitroglycerin ointment) to decrease internal anal sphincter tone has shown promise in the treatment of anal fissure. Anorectal abscesses are categorized into four types: perianal, ischiorectal, intersphincteric, and supralevator. Most are idiopathic and contain mixed aerobic-anaerobic pathogens. Fistula formation varies from 25% to 50% and is much more common with gut-derived organisms (e.g.,E. coli, B. fvngilis). Definitive treatment for an anorectal abscess is timely surgical incision and drainage to prevent more serious complications (e.g., serious infection, extension of the abscess). Anal carcinomas are infrequent, the majority of them being squamom cell or epidermoid carcinomas. The emergency physician must maintain a high index of suspicion and obtain a biopsy of suspicious lesions in order not to miss the diagnosis of a cancer. The most common presenting complaint of anal tumors is rectal bleeding. Combination chemotherapy and radiotherapy have shown promising results in the treatment of anal canal tumors. Bacterial, viral, and protozoal infections can be transmitted to the anorectum via anoreceptive intercourse. Such infections must be considered when a patient presents with rectal pain or discharge, tenesmus, or rectal or perineal ulcers. Proctosigmoidoscopy and rectal cultures may be necessary to determine the cause. Potential rectal complications of HIV infection include infectious diarrhea, acyclovir-resistant strains of HSVZ, Kaposi’s sarcoma, lymphoma, and squamous cell carcinoma. Rectal injuries may result from penetrating or blunt trauma, iatrogenic injuries, or foreign bodies. Rectal injury should be suspected when a patient presents with low abdominal, pelvic, or perineal pain or blood per rectum after sustaining trauma or undergoing an endoscopic or surgical procedure. Tetanus prophylaxis, intravenous antibiotics, and surgical intervention are indicated in all but superficial rectal tears.

References 1. Beahrs OH, Wilson SM: Carcinoma of the anus. Ann Surg 184422, 1976 2. Boman BM, Moertel CG, OConnell MJ, et al: Carcinoma of the anal canal A clinical and pathologic study of 188 cases. Cancer 54:114, 1984 3. Bostick PJ, Johnson DA, Heard JF, et al: Management of extraperitoneal rectal injuries. J Natl Med Assoc 85:460, 1993 4. Brook I, Frazier EH: Aerobic and anaerobic bacteriology of wounds and cutaneous abscesses. Arch Surg 125:1445, 1990

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5. Brown DR, Fife KH: Human papillomavirus infections of the genital tract. Med Clin North Am 74:1455, 1990 6. Christian RL: Anorectal Disorders. In Office Practice of Medicine. Philadelphia, WB Saunders, 1994, p 318 7. Clay LD, White JJ, Davidson JT, et al: Early recognition and successful management of pelvic cellulitis following hemorrhoidal banding. Dis Colon Rectum 29:579, 1986 8. Corey L, Spear PG: Infections with herpes simplex viruses. N Engl J Med 314:749,1986 9. Corman ML: Hemorrhoids. In Colon and Rectal Surgery. Philadelphia, JB Lippincott, 1993, pp 54-115 10. Corman ML: Anorectal abscess and anal fistula. In Colon and Rectal Surrerv. Philadelphia, JB Lippincott, 1993, pp 133-187 11. Daniel GL, Longo WE, Vernava AM: Pruritus ani: Causes and concerns. Dis Colon Rectum 37670, 1994 12. Davidson BS, Simmons GT, Williamson PR, et a1 Pelvic fractures associated with open perineal wounds: A survivable injury. J Trauma 35:36, 1993 13. Davis SM: Disorders of the anorectum. In Rosen P, Barkin RM (eds): Emergency Medicine Concepts and Clinical Practice, ed 3. St. Louis, Mosby, 1992, p 1658 14. Deans GT, McAleer JJA, Spence RAJ: Malignant anal tumours. Br J Surg 81:500, 1994 15. Dennison AR, Whiston RJ, Rooney S, et al: The management of hemorrhoids. Am J Gastroenterol 84:474, 1989 16. Edwards AT, Morus LC, Foster ME, et al: Anal cancer: The case for earlier diagnosis. J R SOCMed 84:395, 1991 17. Eykyn SJ, Grace R H The relevance of microbiology in the management of anorectal sepsis. Ann R Coll Surg Engl 68237, 1986 18. Falcone RE, Wanamaker SR, Santanello SA, et a1 Colorectal trauma: Primary repair or anastomosis with intracolonic bypass vs. ostomy. Dis Colon Rectum 35:957, 1992 19. Ferraro FJ, Livingston DH, Odom J, et a1 The role of sigmoidoscopy in the management of gunshot wounds to the buttocks. Am Surg 59:350, 1993 20. Franko ER, Ivatury RR, Schwalb DM: Combined penetrating rectal and genitourinary injuries: A challenge in management. J Trauma 34:347, 1993 21. Fry RD, Kodner IJ: Anorectal disorders. In Erdelyi-Brown M (ed): Clinical Symposia, vol 37 (no. 6). West Caldwell, NJ, Ciba-Geigy, 37 1985, p 1 22. Fry R D Anorectal trauma and foreign bodies. Surg Clin North Am 74:1491, 1994 23. Fry RD, Kodner IJ: Acute anorectal disorders. In Stine RJ, Chudnofsky CR (eds): A Practical Approach to Emergency Medicine, ed 2. Boston, Little, Brown, and Company, 1994, p 750 24. Glau&r J M Thrombosed external hemorrhoids. In Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine, ed 2. Philadelphia, WB Saunders, 1991, p 704 25. Goldenberg H S Supralevator abscess diagnosis and treatment. Surgery 91:164, 1982 26. Goldstein SD: Anal fissures and fistulas. Postgrad Med 8236, 1987 27. Gorfine SR Treatment of benign anal disease with topical nitroglycerin. Dis Colon Rectum 38:453, 1995 28. Grace RH, Harper IA, Thompson RG: Anorectal sepsis: Microbiology in relation to fistula-in-ano. Br J Surg 69:401, 1982 29. Grosz C R A surgical treatment of thrombosed external hemorrhoids. Dis Colon Rectum 33:249, 1990 30. Gui D, Cassetta E, Anastasio G, et al: Botulinum toxin for chronic anal fissure. Lancet 344:1127, 1994 31. Hakim NS, Sarr MG, Bender CE, et al: Management of barium enema-induced colorectal perforation. Am Surg 58:673, 1992 32. Hancock BD Anal fissures and fistulas. BMJ 304:904, 1992 33. Herr CH, Williams JC: Supralevator anorectal abscess presenting as acute low back pain and sciatica. Ann Emerg Med 23:132, 1994 34. Hillman RJ, Ryait BK, Botcherby M, et al: Changes in HPV infection in patients with anogenital warts and their partners. Genitourin Med 69:450, 1993 35. Huber P, Kissack AS, Simonton CT: Necrotizing soft-tissue infection from rectal abscess. Dis Colon Rectum 26:507, 1982 V

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