26
Perianal Complaints
Stephen F. Lowry and Theodore E. Eisenstat
Objectives
1. To understand the etiologies of and therapeutic approaches to diarrheal diseases.
2. To develop a differential diagnosis for a patient with common perianal disorders (including be- nign, malignant, and inflammatory causes).
3. To discuss the characteristic history and findings for common perianal problems.
4. To discuss a treatment plan for each diagnosis covered by Objective 1, including nonoperative interventions and the role and timing of surgical interventions.
Cases
Case 1
A 48-year-old diabetic man presents with a 2-day history of throbbing perianal pain that is worsened with bowel movement. His temperature is 102°F; his pulse is 108; his blood pressure is 94/50. He has dizziness on standing. Rectal examination reveals a painful, indurated perianal mass. There are no external sinus tracts.
Case 2
A 60-year-old woman presents with a remote history of blood coating her stool. She now has had 12 hours of severe, constant perianal pain.
Examination reveals a tender, purplish subcutaneous mass below the dentate line.
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Anatomy of the Anus
The anatomic anal canal starts at the dentate line and ends at the anal verge. However, a practical definition is the surgical anal canal, which extends from the termination of the muscular diaphragm of the pelvic floor to the anal verge. The anal canal is “supported” by the sur- rounding anal sphincter mechanism, composed of the internal and external sphincters. The internal sphincter is a specialized continuation of the circular muscle of the rectum. The external sphincter is composed of voluntary striated muscle.
Hemorrhoids are found in the subepithelial tissue above and below the dentate line. These are cushions composed of vascular and con- nective tissues and supportive muscle fibers. The middle rectal veins drain the lower rectum and upper anal canal into the systemic system via the internal iliac veins. The inferior rectal veins drain the lower anal canal, communicating with the pudendal veins and draining into the internal iliac veins.
Sensations of noxious stimuli above the dentate line are conducted through afferent fibers of these parasympathetic nerves and are expe- rienced as an ill-defined dull sensation. Below the dentate line, the epithelium is exquisitely sensitive and richly innervated by somatic nerves. The internal sphincter, composed of smooth muscle, generates 85% of the resting tone. It is innervated with sympathetic and parasym- pathetic fibers.
Hemorrhoids are important participants in maintaining conti- nence and minimizing trauma during defecation. They function as protective pillows that engorge with blood during the act of defecation, protecting the anal canal from direct trauma due to passage of stool.
See Algorithm 26.1 for the initial workup of perianal conditions.
Directed history (chief complaint) Anorectal examination
• Inspection
• Palpation
• Digital examination
Anoscopy Proctosigmoidoscopy
Cultures Specimen
collection
Biopsies
Algorithm 26.1. Algorithm for the initial workup of perianal conditions.
Diarrhea: Diagnosis and Management
Diarrhea is defined as liquid stool, rather than soft or formed stool, which has a daily weight exceeding 250 g and is accompanied by excess fluid loss and a number of bowel movements. Four general mechanics are responsible for diarrhea: morphologic alterations of intestinal mucosa, osmotic malabsorption, secretory derangement, and aberrant intestinal motility.
The management of diarrhea begins with a history and physical examination, including a thorough drug, dietary, and travel history as well as questions regarding food ingestion, recent medication changes, exposure to others with diarrhea, and family history. Chronic diarrhea lasts at least 3 to 6 weeks.
All patients with diarrhea should have stool samples tested for fecal leukocytes, occult blood, excess fat, and bacterial cultures. The pres- ence of white blood cells (WBCs) implies an exudative or inflammatory process, usually as a result of an infectious enteritis or inflammatory bowel disease. The presence of blood in the stool without WBCs should arouse suspicion for neoplasm or colonic ischemia. Evaluations for ova and parasites, fecal qualitative fat, or mucosal biopsy are indicated in select cases.
Inflammatory diarrhea is characterized by the presence of fecal leukocytes and persistent diarrhea despite fasting. Infections are the most common cause. Etiologies include viral gastroenteritis (rotavirus), AIDS-related enteritis (giardia, salmonella, cryptosporidium), and pseudomembranous colitis (Clostridium difficile). Assays for C. difficile toxin and visual identification of organisms (giardia) on stain or culture can be diagnostic; antibiotic therapy should be directed against the causative agent. If negative, endoscopy should be performed to directly visualize the mucosa.
Examination of the stool for qualitative fecal fat can help diagnose malabsorption. A 24-hour fecal fat measurement should be ordered;
greater than 10 g of fat per 24-hour period is indicative of malabsorp- tive or maldisgestive steatorrhea.
Exogenous agents that may produce an osmotic diarrhea include laxatives (magnesium sulfate); magnesium-based antacids; dietetic foods with sorbitol, mannitol, or xylitol; and certain drugs used chron- ically (cholestyramine, colchicines, neomycin, and lactulose).
Endogenous sourcesare caused by congenital conditions including disaccharidase deficiencies or generalized malabsorptive/maldigestive processes (cystic fibrosis, congenital lymphangiectasia).
Acquired causes include pancreatic exocrine deficiency, bacterial overgrowth, celiac sprue, bile salt diarrhea, thyrotoxicosis, and adrenal insufficiency. Bacterial overgrowth syndromes can be confirmed by a hydrogen breath test that detects fermentation of carbohydrates by direct measure of hydrogen in the breath. Patients with small-bowel bacterial overgrowth have hydrogen peaks within 3 hours; those with colonic fermentation peak later, thereby identifying the site of the problem.
Secretory diarrheais characterized by watery stools with volumes greater than 1 L per day. Etiologies include enterotoxin-induced secre-
tion (cholera and enterotoxigenic Escherichia coli, diagnosed by toxin identification or organism culture), carcinoid syndrome (serotonin and substance P), pancreatic islet cell tumor syndrome [vasoactive intesti- nal polypeptide (VIP) induced], medullary thyroid carcinoma syn- drome (calcitonin), and Zollinger-Ellison syndrome (gastrin).
Treatment of diarrhea should be directed to the underlying specific cause whenever possible. Treatment of volume depletion is the first step in the management of diarrhea; this can be accomplished in mild cases by avoiding solid foodstuffs and ingesting clear liquids. More severe volume depletion requires intravenous resuscitation.
Benign Diseases
Anorectal Abscess and Fistula
The anal canal has 6 to 14 glands that lie in or near the intersphincteric plane between the internal and external sphincters. Projections from the glands pass through the internal sphincters and drain into the crypts at the dentate line. Glands may become infected when a crypt is occluded, trapping stool and bacteria within the gland. If the crypt does not decompress into the anal canal, an abscess may develop in the intersphincteric plane. The abscess may track within or across the inter- sphincteric plane. Abscesses are classified by the space they invade (Fig. 26.1). Regardless of abscess location, the extent of disease often is difficult to determine without examination under anesthesia.
Antibiotics given while allowing the abscess to “mature” are not helpful. Early surgical consultation and operative drainage are the
Figure 26.1. Abscesses are classified by location. (Reprinted from Vasilevsky CA. Fistula-in-ano and abscess. In: Beck DE, Wexner SD, eds. Fundamentals of Anorectal and Colonic Diseases, 2nd ed. New York: McGraw-Hill, 1992, with permission.)
best measures to use to avoid the disastrous complications associated with undrained perineal sepsis. When drained either surgically or spontaneously, 50% of abscesses have persistent communication with the crypt, creating a fistula from the anus to the perianal skin or fistula in ano. A fistula in ano is not a surgical emergency because the septic focus has drained.
As in Case 1, an abscess typically causes severe, continuous, throb- bing anal pain that may worsen with ambulation and straining.
Occasionally, patients present with fever, urinary retention, and life- threatening sepsis, which especially is true in diabetics and the immunocompromised host.
Physical examination of the patient with an abscess reveals a tender perianal or perirectal mass. No imaging studies are necessary in uncomplicated abscess fistulous disease, but imaging studies such as sinograms, transrectal ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) may be useful in the evaluation of complex or recurrent disease. An approach to surgical management of perianal abscesses/fistulas is shown in Algorithm 26.2.
Abscess fistula disease of cryptoglandular origin must be differ- entiated from complications of Crohn’s disease, pilonidal disease, hidradenitis suppurativa, tuberculosis, actinomycosis, trauma, fissures, carcinoma, radiation, chlamydia, local dermal processes, retrorectal tumors, diverticulitis, and ureteral injuries. Five percent to 10% of patients with Crohn’s disease initially present with anorectal abscess or fistulous disease. A colonic source may be suspected in a patient with known inflammatory bowel disease or diverticular disease.
The complications of an undrained anorectal abscess may be severe.If the abscess is not drained surgically or spontaneously, the infection may spread rapidly, which may result in extensive tissue loss, sphincter injury, and even death. Abscesses should be drained surgi- cally. Patients often require drainage in the operating room, where anesthesia allows for adequate evaluation of the extent of the disease.
Physical exam
Anterior (straight course)
Posterior (curves to posterior midline)
Superficial
Deep
Rectovaginal
Superficial
Deep
Fistula Seton Rectal flap Transvaginal Transrectal Transperineal
Fistulotomy Seton Rectal flap Algorithm 26.2. Algorithm for an approach to the surgical management of perianal abscesses/fistulas.
Patients with a chronic or recurring abscess after apparent adequate surgical drainage often have an undrained, deep, postanal space abscess that communicates with the ischiorectal fossa via a “horseshoe fistula.” Immunocompromised patients are a particular challenge, as seen in Case 1. These patients are more prone to necrotizing anorectal infections.
The treatment of fistulas is dictated by the course of the fistula.
Goodsall’s rule is of particular assistance in identifying the direction of the tract (Fig. 26.2) in fistulas with posterior external openings, but reliability is decreased anteriorly and in particular as the distance from the verge is increased.
Anal Fissure/Ulcer
An anal fissure is a split in the anoderm. An ulcer is a chronic fissure.
Fissures most frequently occur in the midline just distal to the dentate line. Fissures result from forceful dilation of the anal canal, most com- monly during defecation. Classically, the initial insult is believed to be a firm bowel movement. The pain associated with the initial bowel movement is great, and the patient therefore ignores the urge to defe- cate for fear of experiencing the pain again. A self-perpetuating cycle of pain, poor relaxation, and reinjury results.
Fissures cause pain and bleeding with defecation. The pain is often tearing or burning, worse during defecation, and subsides over a few hours. Anoscopy and proctosigmoidoscopy should be deferred until healing occurs or the procedure can be performed under anesthesia.
Although anoscopy and rigid sigmoidoscopy may not be performed Figure 26.2. Goodsall’s rule: External openings anterior to a line drawn between the 3 and 9 o’clock positions communicate with an internal opening along a straight line drawn toward the dentate line. Posterior external open- ings communicate with the posterior midline in a nonlinear fashion. The exception may be an interior opening that is greater than 3 cm from the dentate line. (Reprinted from Marti M-C, Givel J-C, eds. Surgical Management of Anorectal and Colonic Diseases, 2nd ed. Heidelberg: Springer-Verlag, 1999, with permission.)
in the initial evaluation of a patient with a fissure, they must be per- formed during a subsequent visit because the presence of associated anorectal malignancy or inflammatory bowel disease must be excluded.
Ulcers occurring off the midline or away from the mucocutan- eous junction are suspect. Crohn’s disease, anal TB, anal malignancy, abscess/fistula disease, cytomegalovirus (CMV), herpes, chlamydia, syphilis, AIDS, and some blood dyscrasias all may mimic certain aspects of fissures/ulcer disease.
Treatmentusing stool softeners, bulk agents, and sitz baths is suc- cessful in healing 90% of anal fissures. Patients are instructed to soak in a hot bath and contract the sphincters to identify the muscle in spasm and then focus on relaxing that muscle. Botox infiltration into the inter- nal sphincters may be effective in the treatment of anal fissures. Lateral internal sphincterotomy is the procedure of choice for many surgeons after conservative measures have failed.
Hemorrhoids
Patients with perianal pathology often present or are referred with a chief complaint of “hemorrhoids.” A thorough history frequently sug- gests the diagnosis. Those individuals with painless bleeding due to hemorrhoids must be distinguished from those with bleeding from colorectal malignancy, inflammatory bowel disease, diverticular disease, and adenomatous polyps. Rectal prolapse must be distin- guished from hemorrhoids because it is safe to band a hemorrhoid but not a prolapsed rectum.
Hemorrhoidal tissues are part of the normal anatomy of the distal rectum and anal canal. The disease state of “hemorrhoids” exists when the internal complex becomes chronically engorged or the tissue pro- lapses into the anal canal as the result of laxity of the surrounding con- nective tissue and dilatation of the veins. External hemorrhoids may thrombose, leading to acute onset of severe perianal pain. An approach to the management of hemorrhoid disease is shown in Algorithm 26.3.
Internal hemorrhoids may have two main pathophysiologic mecha- nisms seen in two distinct but not exclusive groups: older women and younger men. Internal hemorrhoids originate above the dentate line and are lined with insensate rectal columnar and transitional mucosa.
In older women, the pathophysiologic mechanism may be related to earlier pregnancy or chronic straining, which leads to vascular engorgement and dilatation, resulting in stretching and disruption of the supporting connective tissue surrounding the vascular channels.
Another suggested pathologic mechanism, and the one that may be more important in younger men, is that of increased resting pressures within the anal canal, leading to decreased venous return. Internal hemorrhoids typically do not cause pain but rather bright-red bleed- ing per rectum, mucous discharge, and a sense of rectal fullness or discomfort.
External hemorrhoids may develop an acute intravascular thrombus, which is associated with acute onset of extreme perianal pain. The pain
usually peaks within 48 hours. Repeated episodes of dilatation and thrombosis may lead to enlargement of the overlying skin, which is seen as a skin tag on physical exam. As in Case 2, the acutely throm- bosed external hemorrhoid is seen as a purplish, edematous, tense sub- cutaneous perianal mass that is quite tender.
The complications of internal or external hemorrhoids are the indi- cations for medical or surgical intervention: bleeding, pain, necrosis, mucous discharge, moisture, and, rarely, perianal sepsis. Initial medical management for all but the most advanced cases is recommended.
Dietary alterations, including elimination of constipating foods (e.g., cheeses), addition of bulking agents, stool softeners, and increased intake of liquids are advised. Internal hemorrhoids that fail to respond to medical management may be treated with elastic band ligation, scle- rosis, photocoagulation, cryosurgery, excisional hemorrhoidectomy, and many other local techniques that induce scarring and fixation of the hemorrhoids to the underlying tissues. The acutely thrombosed external hemorrhoid may be treated with excision of the hemorrhoid or clot evacuation if the patient presents within 48 hours of onset of symptoms. If the patient presents more than 48 hours after onset of symptoms, conservation management with warm sitz baths, high-fiber diet, stool softeners, and reassurance is advised.
Pilonidal Disease
Patients with pilonidal disease may present with small midline pits or an abscess(es) off the midline near the coccyx or sacrum. The workup is limited to a physical exam unless one suspects Crohn’s disease; then
Initial assessment
• History
• Exam
• Classification Internal
External
Determine severity
Thrombectomy, if thrombosed Improve hygiene
Topical agents
Grade 1 Grade 2
Grade 3
Grade 4
Rubber banding Infrared coagulation Sclerotherapy Diet changes
Consider nonsurgical therapy
Surgery
Failed
Failed
Failed Surgery
Repeat as needed
Failed
Surgery
Special circumstances
• Pregnancy
• Inflammatory bowel disease
Algorithm 26.3. Algorithm for an approach to the management of hemorrhoid disease.
a more extensive evaluation may be necessary. The differential diag- nosis includes abscess/fistulous disease of the anus, hidradenitis sup- purativa, furuncle, and actinomycosis.
Pilonidal abscesses may be drained under local anesthesia. For those who fail to heal after 3 months or develop a chronic draining sinus, definitive therapy is recommended. The preferred method is to excise the pilonidal disease and primarily close the defect with rota- tional flaps over closed suction drainage. Simple primary closure has an unacceptably high dehiscence rate.
Neoplasms
Historically, the anal canal has been defined as the region above the dentate line, and the anal margin has been defined as the area below the dentate line. Squamous cell tumors of the anal margin are well dif- ferentiated, keratinizing tumors that behave similarly to squamous cell tumors of the skin elsewhere. Tumors of the anal canal are aggressive, high-grade tumors with significant risk for metastasis. The staging system for anal tumors is shown in Table 26.1.
Tumors of the Anal Margin Squamous Cell Carcinoma
Patients frequently complain of a lump, bleeding, itching, pain, or tenesmus (complaints common to most lesions of this region). Typi- cally, the lesions are large, are centrally ulcerated with rolled everted
Table 26.1. Staging for anal cancer.
Anal Canal
T1 £2cm
T2 >2 to 5cm T3 >5cm
T4 Adjacent organ(s) N1 Perirectal
N2 Unilateral internal iliac/inguinal
N3 Perirectal and inguinal, bilateral internal iliac/inguinal Stage Grouping
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
T3 N0 M0
Stage IIIA T1 N1 M0
T2 N1 M0
T3 N1 M0
T4 N0 M0
Stage IIIB T4 N1 M0
Any T N2, N3 M0
Stage IV Any T Any N M1
Source: Reprinted from Welton ML, Varma MG, Amerhauser A. Colon, rectum, and anus.
In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
edges, and have been present for more than 2 years before detection.
All chronic or nonhealing ulcers of the perineum should be biopsied to rule out squamous cell carcinoma.
Tumors of the Anal Canal Epidermoid Carcinoma
Generally, there is a long history of minor perianal complaints such as bleeding, itching, or perianal discomfort. Early lesions that are small, mobile, confined to the submucosa, and well differentiated may be treated with local excision. Radiation therapy or chemora- diotherapy is the preferred treatment option for larger lesions of the anal canal.
Summary
Patients with perianal problems often are referred with a diagnosis of hemorrhoids. The sometimes life-threatening causes of perianal complaints require attention to history and a thorough physical examination. While hemorrhoidal disease often can be treated expectantly or by local therapies, improperly treated infectious and malignant causes of such complaints often result in devastating consequences.
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