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Author: Laurence Scott Bailen, M.D.
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1. Objectives: Benign Colon Disorders

  1. Understand the mechanism of defecation

  2. Understand the causes of constipation

  3. Understand how colonic diverticula form

  4. Understand there are two common complications from colonic diverticulosis: diverticulitis (inflammation and infections) and diverticular bleeding

  5. Understand the common symptoms associated with acute appendicitis recognizing that in certain situations (pregnancy, elderly individuals) the symptoms may be different

  6. Understand how hemorrhoids develop and how they are treated

  7. Understand how anal fissures develop and how they are treated

  8. Understand the clinical situations in which an anorectal abscess or fistula develops and the associated symptoms

2. Constipation

2.1. Epidemiology

Constipation is a frequent problem among people in the western world. Constipation most commonly affects children and the elderly. Symptoms of constipation are reported by 5-30% of the United States population based on large surveys. Constipation is more commonly reported in women than men and in non-whites compared to whites. The prevalence in both age and race situations rises with age, being more common over age 60. Laxative use also increases with age: in one population survey 6.8% of people 65 and over reported taking at least 3-10 laxatives each week and 6.4% reported using enemas. Among young adults, 3.4% reported using laxatives at least once per month. The cost of treating constipation is high given that over 2.5 million office visits to physicians per year are related to symptoms of constipation.

2.2. Symptoms of Constipation

The concept of constipation differs among people; therefore it is important to ask the patient what they mean by “constipation." Symptoms associated with the term constipation include:

  • Infrequent stools

  • No urge to defecate

  • Stools difficult to pass - straining

  • Need to digitally remove stool

  • Sense of incomplete evacuation

  • Soiling of clothes

  • Bloating

  • Abdominal discomfort or pain

2.3. Definition of Constipation:

Two or more of following symptoms for at least 3 months:

  • Straining more than 25% of time

  • Hard stools more than 25% of time

  • Incomplete evacuation more than 25% of time

  • Less than 3 bowel movements per week

2.4. Function of Colon

The primary functions of the colon are storage and conversion of liquid stool to solid feces and the elimination of fecal contents. Through the active absorption of water and electrolytes, the activities of colonic microflora, and colonic motility the ~1500cc of liquid that enter the colon is converted into ~200g of solid stool per day.

In the proximal colon, from the ileo-cecal valve to the hepatic flexure, feces is mixed by segmental and retrograde contractions which slow fecal passage and allow time for fluid absorption. This area serves as an important reservoir. In the distal colon, from the hepatic flexure to the recto-sigmoid junction, orthograde contractions move feces to the rectum and allow for further fluid resorption. Several times per day (2-3 times) there is a large propulsive peristaltic movement which propels feces into the rectum. The rectum is primarily a storage site and fills slowly until defecation is convenient.

Defecation is a complex process. It involves the interplay of autonomic and voluntary mechanisms. The pelvic floor musculature aid in continence as they form a sling around the rectum to maintain an acute anorectal angle. (See Figure 1 : Image not available due to copyright restrictions). These muscles are primarily innervated by the pudendal nerve. The internal anal sphincter (IAS) is under autonomic, involuntary control and is tonically contracted. When the rectum is distended the IAS relaxes, defecation is initiated and there is voluntary relaxation of the external anal sphincter. At the same time the pelvic floor muscles relax, the perineum descends, and the acute anorectal angle straightens allowing for evacuation. “Bearing down” or “straining” is a valsalva maneuver which increases intraabdominal pressure to aid in evacuation.

2.5. General Thoughts on the Pathophysiology of Constipation

General factors :

  • Sex: more common in women than men (reason unclear – no associated with sex hormones

  • Age: more common in elderly based on less food intake, reduced mobility, weaker abdominal and pelvic muscles, medications

  • Diet: correlation with fiber intake controversial in population surveys but fiber tends to increase colonic transit time.

Colonic anatomy and function :

  • Luminal contents – less fiber may reduce colonic transit time

  • Absorption of water and sodium – a long colon and wide colon increases time and surface area for water absorption therefore reducing stool size.

  • Diameter and length of colon

  • Colonic motor function

  • Defecatory dysfunction

    • Failure of relaxation of anal sphincter

    • Ineffective straining

    • Diminished rectal sensation

Psychological factors

2.6. Causes of Constipation

  • Modes of life

    • Inadequate fiber

    • Little food intake

    • Ignoring urge to defecate (children)

    • Immobility (elderly)

  • Drugs

    • Opiates

    • Anti-cholingerics

    • Anti-depressants

    • Anti-convulsants

  • Metabolic/Endocrinologic

    • Hypothyroidism

    • Hypercalcemia

  • Neurologic

    • Parkinson’s disease

    • Multiple Sclerosis

    • Spinal lesions

    • Autonomic neuropathy

  • Gastrointestinal tract

    • Luminal obstruction

    • Aganglionosis (Hirschsprung’s disease)

    • Myopathy

    • Neuropathy

    • Systemic sclerosis (scleroderma)

  • Anorectum

    • Anal atresia

    • Anal stenosis

    • Large rectocele

    • Weak pelvic floor

    • Rectal prolapse

  • Idiopathic constipation

    • Irritable bowel syndrome

    • Slow colonic transit (colonic inertia)

    • Outlet delay:

      • Megarectum

      • Fecal impaction

      • Pelvic floor dyssynergia

      • Hirschsprung’s disease (congenital aganglionosis in rectum/distal sigmoid)

    • Pseudoobstruction

2.7. Clinical Evaluation of Constipation

  • History including obstetric history

  • Past history

  • Drug history

  • Physical examination – including digital rectal examination

  • Diary card

2.7.1. Investigations

  1. Tests to exclude systemic disease: Hemoglobin, erythrocyte sedimentation rate, thryoid function, calcium.

  2. Tests to exclude structural disease of gut:

    1. Barium x-rays

    2. Colonoscopy

  3. Measurement of colonic transit (See Figure 2 )

    1. Markers study – patient ingests radioopaque markers (pellets) and 5 days later a plain abdominal film is obtained. >80% of markers should be expelled by this time.

      1. Modifications – check radiographs at 72, 96, and 120 hours after administration to assess transit through different colon segments: primarily helpful in diagnosing outlet delay (Hirschsprung’s, megarectum, pelvic floor dyssynergia) where markers are retained in rectum.

  4. Defecography

  5. Anorectal manometry

  6. Electromyography

Figure 2. Colonic Transit Study – Image not available due to copyright restrictions

2.8. Treatment of Constipation

  1. General

    1. Reassurance

    2. Mode of life – make time for defacation

    3. Psychological support – stress management

    4. Diet 0 increase fiber in diet

    5. Fluid intake – increase

  2. Laxatives

    Class

    Chemical Makeup

    Mechanism of Action

    Examples

    Possible Side Effects

    Bulk laxatives

    Concentrated form of non-starch polysaccharides

    Increase fecal bulk

    Methimazole

    Methylcellulose Powder

    Possible allergic reactions (rare)

    Unabsorbed sugars

    Synthetic disaccharides

    Sugars not absorbed in small bowel, fermented in colon –stimulate colon secretion

    Lactulose

    Very sweet taste

    Abdominal distension

    Salts

    Sodium sulfate, magnesium citrate

    Magnesium and sulfate are poorly absorbed ions

    Magnesium citrate

    Hypermagnesemia

    Anthranoid compounds

    Plant glycosides

    Glycosides activated in colon by bacteria and cause increased colon secretion and motility

    Senna, aloe, cascara, frangula

    Melanosis coli

    ?cathartic colon

    Polyphenolic compounds

    Polyphenols

    Increased colon motility and secretion

    Phenolphthalein(PP)(not available anymore), bisacodyl

    Rash (PP)

    Detergents

    Dioctyl sodium sulfosuccinate

    Stool softener – increases fluid secretion

    Docusate sodium

    Liquid paraffin

    Mineral oil

    Softens stools

    Mineral oil

    Aspiration can cause lipoid pneumonia

    Prokinetic drugs

    Cisapride

    Cisapride

    No role in routine management

    Unabsorbed fluid

    Polyethylene glycol

    Electrolyte solution – osmotic action

    PEG-ES


  1. Enemas and suppositories

    • →Saline enemas act by distention

    • →Hypertonic sodium phosphate emenas at by distention and stimulation (be aware of hyperphosphatemia)

    • →Stimulant suppositories or enemas – glycerin, bisacodyl (available in oral and rectal formula)

3. Diverticular Disease of the Colon

3.1. Epidemiology

Incidence of diverticula higher in societies with low intake of dietary fiber. Therefore, there is a high incidence of diverticular disease in the United States and a relatively low incidence in Asian populations. Diverticular disease is acquired therefore the incidence increases with older age. Diverticula are rare in patients younger than 40 and approaches 50% incidence by the ninth decade of life.

The anatomic distribution of diverticula also varies with geographic location. Generally, industrialized countries with a Western diet have predominantly left sided diverticulosis (in the sigmoid and descending colon). Right sided diverticulosis is more common in Asian patients.

3.2. Pathogenesis

Multifactorial: related to colon anatomy, alterations of colon wall with aging, motor dysfunction, increases in intraluminal pressure, low dietary fiber.

3.3. Pathology and Functional Abnormalities

The most common diverticula are more accurately referred to as pseudodiverticula which are herniations of the mucosa and submucosa through the muscularis of the colon. True diverticula containing all layers of the bowel wall are rare. (This section will refer to pseudodiverticula as diverticula). Diverticula develop in rows between the mesenteric and lateral or anti-mesenteric teniae. The points of greatest weakness in the colon wall is where the intramural vasa recta penetrate the circular muscle to the submucosa. (See Figure 3 – Image not available due to copyright restrictions). Subsequently the circular muscle layer and the outer longitudinal muscle layer are thickened. This leads to shortening of the teniae, narrowing of the colonic lumen which allows muscle contractions to obliterate the lumen, dividing the colon into isolated segments. This hypersegmentation (See Figure 4 – Image not available due to restrictions) leads to increased intramluminal

pressure by transmitting the motor work of the colon musculature to the bowel wall rather than to propelling stool. These high pressures lead to further mucosal herniation.

3.4. Diverticulosis: Clinical Manifestations

Most patients are asymptomatic. Some may complain of intermittent abdominal pain or bloating. If the colon is sufficiently narrowed by numerous diverticula the caliber of the stool may be altered – in this situation one must rule out colon carcinoma.

  1. Diagnostic tests → barium enema; colonoscopy

  2. Treatment → high fiber diet; rarely surgery

3.5. Diverticular Bleeding

Painless rectal bleeding occurs in 15-40% of patients with diverticulosis. Usually, the bleeding stops on its own. However, in 5% of cases the bleeding is massive and surgery is required to remove the involved segment of colon. Bleeding is felt to be due to chronic injury to the vasa recta adjacent to the lumen of the diverticula.

Diagnostic studies include colonoscopy, angiography, nuclear medicine techniques (radiolabeled red blood cell scans). Barium x-rays have no place in the evaluation or management of acute diverticular bleeding.

Treatment is usually supportive (intravenous fluids, monitoring hematocrit, transfusing blood as necessary) as most bleeding stops spontaneously. Surgery is necessary for intractable bleeding.

3.6. Diverticulitis

Diverticulitis results from inflammation and perforation of a diverticulum. This complication occurs in 10-25% of patients with diverticulosis. Diverticulitis occurs due to a microperforation of the diverticulum due to impissated stool in the diverticulum causing abrasions to the mucosal lining of the diverticula. After a microperforation occurs inflammation develops in the peridiverticular area which is contained by the pericolonic fat. The inflammatory process can grow into the mesentary and develop into an abscess. A macroperforation may also occur which can result in generalized peritonitis or fistula formation (connections between colon and other organs i.e., bladder, vagina, skin, or other loops of bowel.

Patients classically present with fever and left lower quadrant abdominal pain (as most diverticula in people from western societies occur in the sigmoid colon). Patients are often exquisitely tender in the left lower quadrant on physical examination and have a prominent leukocytosis on blood work.

An abdominal CT scan is the most helpful radiologic test in the evaluation of patients with suspected diverticulitis. This x-ray may show inflammatory activity in the mesentary or an abscess or a fistula.

Treatment in cases of uncomplicated (no abscess, fistula, peritonitis) diverticulitis is usually with antibiotics and supportive care. Younger (<age 40) patients with diverticulitis may have a more aggressive course and should be considered for surgical resection of the involved colon. Treatment of complicated diverticulitis involves antibiotics and surgery.

4. Appendicitis

4.1. Epidemiology

Acute appendicitis is the most common surgical abdominal emergency. 5-10% of the population will develop this at some point in their lives. The peak incidence is in the second and third decades.

4.2. Anatomy

The appendix projects from the apex of the cecum. It may lie in a retrocecal, subcecal, pelvic, post-ileal, or pre-ileal position. ( Figure 5 – Image not available due to copyright restrictions)

The function of the appendix is unknown but an immunologic action is hypothesized based on the abundance of lymphoid tissue in the appendiceal wall.

4.3. Pathogenesis

Appendicitis develops from the obstruction of the lumen by fecaliths (small bits of feces) with subsequent mucosal ischemia and bacterial infection of the appendiceal wall. This eventually leads to perforation and extension of the infectious process. In 1/3rd of patients the inflammed appendix has no obstructing lesion – the pathogenesis of appendicitis in these patients is unclear and controversial.

4.4. Diagnosis

Clinical history: 1) pain at some site in the abdomen, classically near the umbilicus then 2) anorexia, nausea and vomiting then 3) pain over the appendix in the right lower quadrant (McBurney’s point) then 4) fever.

This history varies in patients with a retrocecal appendix (pain less intense and symptoms vague), in elderly patients (symptoms are vague, pain minimal, and fever only slightly elevated), in pregnant women, and in an immunosuppressed patient.

Imaging studies – none required if history and physical exam consistent. Barium enemas and ultrasound can aid in the diagnosis as can a CT scan.

4.5. Treatment

Surgical removal by open or laparoscopic techniques.

5. Hemorrhoids

Hemorrhoids are masses of vascular tissue in the anal canal containing a rich arteriovenous network. They are normally present at birth as they help maintain continence by partially occluding the anus. Hemorrhoids become symptomatic when they become enlarged and dilated. Internal hemorrhoids arise from the superior (internal) hemorrhoidal vascular plexuses and are covered by mucosa (therefore not painful). External hemorrhoids are dilations of the inferior (external) hemorrhoidal plexuses and are covered by anoderm and perianal skin (therefore painful). See Figure 6 .

Figure 6: Anorectal Anatomy

Anorectal anatomy
Anorectal anatomy

5.1. Epidemiology

Enlarged hemorrhoidal tissue is present in approximately 50% of the adult population in the United States. Enlarged hemorrhoids are symptomatic in approximately 10-25% of these individuals.

5.2. Internal Hemorrhoids: Classification

  1. First degree: project slightly into the anal canal and the only symptom is bleeding

  2. Second degree: prolapse with defecation out into the anal canal but reduce (back into rectum) spontaneously

  3. Third degree: prolapse with defecation but must be reduced manually

  4. Fourth degree: prolapse and can not be reduced

5.3. Symptoms and Physical Exam Findings

Patients with internal hemorrhoids will experience painless bright red bleeding per rectum. This bleeding usually occurs with a bowel movement. There may be streaks of blood on toilet paper or on the surface of the stool. Blood may drip after passage of a bowel movement. A small amount of blood in the toilet bowl may seem like a lot of blood to patients. When internal hemorrhoids prolapse the patient will sense a mass of tissue protruding from the anus with defecation. Pain is not a symptom of internal hemorrhoids. If hygiene is poor, internal hemorrhoids which prolapse may cause some itching. Patients may have a mucoid discharge if the prolapse is 3rd or 4th degree.

On physical exam, internal hemorrhoids are not palpable on digital rectal exam (they are filled with blood and collapse easily). Anoscopy needs to be performed to accurately determine whether or not hemorrhoids are present. On anoscopic exam, hemorrhoids appear as large bluish tissue which bulge into the lumen.

External hemorrhoids become symptomatic when they thrombose and are covered by anoderm or perianal skin. Patients with external hemorrhoids experience pain and bleeding. On physical examination, the external hemorrhoid will be extremely tender to touch.

5.4. Pathogenesis of Hemorrhoids

Hemorrhoids develop from a combination of factors. Hemorrhoidal tissue is repeatedly subject to downward pressure during defecation. Over time, the muscle fibers that anchor the hemorrhoidal tissue loosen which causes the hemorrhoidal tissue to slide, become congested, and eventually bleed.

5.5. Treatment of Hemorrhoids'

Rationale

Treatment

Reduced downward pressure

Diet, stool bulking agents (fiber)

Avoid prolonged sitting at defection

Fix cushions to underlying sphincter

Sclerosants

Rubber band ligation

Cryotherapy

Photocoagulation

Electrocoagulation

Reduce anal and sphincter pressure

Manual dilation

Internal sphincterotomy (surgery)

Excise hemorrhoids

Hemorrhoidectomy (surgery)

6. Anal Fissures

Anal fissures are longitudinal or elliptical tears or defects in the anal canal. They are typically seen in young – middle aged individuals. They are typically caused by excessive straining when passing stool which causes trauma to the anal canal. Anal fissures, however, may also be associated with Crohn’s disease or anal carcinoma. Most (98%) of anal fissures are located in the posterior midline. Those not located in the posterior midline are often due to Crohn’s disease or carcinoma. The cardinal symptom of an anal fissure is exquisite pain in the anal area usually exacerbated on defecation. Anal fissures may also bleed. An anal fissure may be chronic and cause persistent pain. In this situation, physical examination will show the anal fissure, a hypertrophied anal papilla at the proximal end of the fissure, and a sentinel tag at the distal end. Treatment of acute anal fissures involves sitz baths, fiber stool bulking agents, lubricating suppositories. Sometimes, topical nitroglycerin is used and may lead to substantial pain relief – however, a common side effect is headache. It may take 4-8 weeks for a fissure to heal. If a fissure does not heal other measures for treatment including botulinum toxin injections into the anal sphincter or surgery may be necessary.

7. Anorectal Abscesses and Anorectal Fistula

Anorectal abscesses are infections of tissue spaces adjacent to the rectum and anal canal (see Figure 7 ). Certain conditions predispose to the development of an anorectal abscess:

  • Crohn’s disease

  • Hematologic disorders

  • Immunodeficiency states

Patients with an anorectal abscess will experience pain, fever, and the sensation of a mass in the anorectal area. Treatment of anorectal abscesses involves surgical drainage and antibiotics.

Figure 7. Anorectal abscesses – Image not available due to copyright restrictions

An anorectal fistula is a hollow fibrous tract lined by granulation tissue. The internal opening of the fistula is located in the rectum or the proximal anal canal and the external opening is on the skin (see Figure 8 ). An anorectal fistula will drain pus, blood, mucus, and stool. It can be very painful. Disorders associated with anorectal fistulae include:

  • Crohn’s disease

  • Rectal or anal cancer

  • Prior radiation treatments to area to treat another condition (prostate cancer, vaginal cancer, vulvar cancer, anal cancer)

The treatment of an anorectal fistula involves antibiotic therapy and often surgical excision.

Figure 8. Anorectal Fistual – Image not available due to copyright restrictions