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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Benign tumors of the colon and rectum

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This chapter consists of three parts of different benign lesions of the colon and rectum (Crawford 1994) (table I):

Table I. Lesions of the Colon and Rectum.

Table I

Lesions of the Colon and Rectum.


Non-neoplastic epithelial polyps


Neoplastic epithelial polyps


Mesenchymal lesions

For information of neuroendocrine tumors (“carcinoids”) the reader is referred to chapter #87 and for more details about the familial adenomatous polyposis coli (FAP) and the adenoma-carcinoma-sequence to chapter #28+29 (Vogelstein 1990).

  • A polyp is a well circumscribed tissue mass that protrudes into the lumen of the colon. Traction on the mass may create a pedunculated polyp. Alternatively the polyp may be sessile.
  • Polyps may be formed as a result of abnormal mucosal maturation, inflammation or architecture. These polyps are non-neoplastic (no malignant potential).
  • Those epithelial polyps that arise as the result of proliferative dysplasia are termed adenomatous polyps or adenomas. They are true neoplastic formations and are premalignant lesions.
  • Polypoid lesions may be caused by mesenchymal submucosal or mural tumors (Crawford 1994).


The majority of intestinal polyps occur on a sporadic basis and increase in frequency with age.

Hyperplastic polyps

In England hyperplastic polyps are called metaplastic. These epithelial polyps have usually a diameter of less than 5 millimeters. They are found in the rectum and sigmoid often at the summit of mucosal folds and valves. Nearly always they occur in a multiple manner. Individuals are asymptomatic. On endoscopic examination they appear in the same color as the rectal mucosa. There is a suggestion that the cells forming the hyperplastic polyps grow more slowly and have a longer lifespan than adjacent normal mucosa cells. Hyperplastic polyps have virtually no malignant potential.

In a study, diagnostic sensitivity of detecting adenomas was 69%, while specificity (the accurate diagnosis of hyperplastic polyps) was 86% (Goodman 1998, Neale 1987).

One of multiple hyperplastic polyps should be excised to confirm the true nature of the lesion.


A hamartoma is composed of an abnormal mixture of normal tissue (Crawford 1994). They may occur sporadically or be associated with the rare autosomal dominant juvenile polyposis syndrome.

Juvenile polyps

Juvenile polyp (congenital polyp, retention polyp, juvenile adenoma) usually occurs in children under ten years of age (Morson 1962). The incidence in boys (men) is higher (Roth, 1963) than in girls (women). It is the most frequent colorectal tumor in children. Nearly 80% occur in the rectum but they may be scattered throughout the colon (Mazier 1982, Jalihal 1992). The majority of these polyps are larger than 1 cm in diameter. The section surface shows a cystic appearance with spaces filled with mucous.

Diagnosis is confirmed by histology of the endoscopically resected polyp. In case of a juvenile polyp the whole colon should be explored (cp. below). A juvenile polyp is neither a neoplasm nor a premalignant condition. Once the single polyp is removed no further follow-up is required.

Juvenile polyposis syndrome is an uncommon condition in which multiple juvenile polyps arise in the colon but also in the intestinal tract. There is a family history in about 20 to 50% of patients (Rickert 1979). The recurrence rate of solitary juvenile polyps is < 20% whereas the rate in familial cases is nearly 90% (Haggitt 1970). Symptoms and signs are hematochezia, iron deficiency anemia, hypoproteinemia, hypokalemia, anergy (Grosfield 1986). There are extracolonic congenital and acquired manifestations as macrocephaly, alopecia, bony swellings, cleft lip, cleft palate, double renal pelvis and ureter, acute glomeronephritis undescended testicle and bifid uterus and vagina (Desai 1995). A fatal form of juvenile polyposis in infancy is characterized with profuse diarrhea, protein losing enteropathy, bleeding and rectal prolapse (Desai 1995). This form is very rare. The appearance of the disease is associated with benign and malignant neoplasms of the gastrointestinal tract. In most cases this disease is identified in childhood.

As juvenile polyposis is considered a potential premalignant condition an aggressive management is indicated (Longo 1990). All juvenile polyps should be resected by means of colonoscopy. If there are too many polyps, restorative proctocolectomy with ileal pouch should be considered. Because of the ileal reservoir neoplasms a follow-up of periodic endoscopy together with the upper gastrointestinal tract should be initiated. An index person indicates colorectal evaluation of the family members.

Peutz-Jeghers’ polyps

Peutz-Jeghers’ polyps occur singly or multiple in the Peutz-Jeghers’ syndrome which is a rare autosomal dominant disease. Multiple polyps scattered throughout – the entire gastrointestinal tract and melanotic mucosal and cutaneous pigmentation around the lips, oral mucosa, face, genitalia and palmar surfaces of the hands (Robbins 1994). They tend to be large and pedunculated, histologically, it’s an network of connective tissue and well developed smooth muscle extending into the polyp. In 100% these polyps occur in the small bowel (colon 30%, stomach 25%) (Crawford 1994). Diagnosis of the syndrome is based on family history, skin pigmentation and gastrointestinal symptoms. The most common signs are abdominal pain often due to intestinal obstruction (polyps themselves or an intussusception). Rectal bleeding is another frequent symptom. Contrast studies and endoscopy show the extend of the disease. The histological work-up suggests a lesion representing a hamartomatous process or malformation rather than a neoplasm (Morson 1962). Solitary Peutz-Jeghers’ polyps in the colon may be resected by colonoscopy. This because the focus organs of the polyps concerning frequency are the duodenum and the small intestine. The small intestinal polyps may be resected during laparotomy by means of endoscopes or enterotomy. An aggressive approach for endoscopic removal is justified because the frequency of tumors decreases as the patients become older (Goodman 1998). Bowel resection should be indicated restrictively.

Juvenile polyps themselves do not have malignant potential. These patients have an increased risk of developing carcinomas of the pancreas, breast, lung, ovary and uterus (Boardman 1998, Giardiello 1987). Gastrointestinal adenocarcinomas in this disease arise from concomitant adenomatous lesion (Crawford 1994, Konishi 1987). Their most common sites are located in the colon and rectum (Konishi 1987).

The differentiation between juvenile and adenomatous polyps is essential. Because of the increased incidence of cancers in other organs (cp. above), these patients need a careful follow-up with frequent clinical examination, abdominal and endovaginal ultrasound, chest-radiograph and mammography (Shields 1987) (this note is not evidence based!).

Inflammatory polyps

Inflammatory (pseudo-) polyps representing nubbins of inflamed regenerating mucosa surrounded by ulceration, are seen in patients with long standing inflammatory bowel disease (ulcerative colitis or Crohn’s disease) (Crawford 1994).

Lymphoid polyps

A lymphoid polyp (lymphoid hyperplasia, benign lymphoma) is a benign, focal or diffuse condition that occur typically where clusters of lymphoid follicles are present (terminal ileum, rectum) (Corman 1998). A lymphoid polyp is characterized radiographically by small, uniform localized or generalized polypoid lesions. Endoscopic examination with biopsy confirms the nature of the polyp. The polyp is composed of well differentiated lymphoid tissue. Rectal lesions may lack symptoms while colonic polyps may cause bleeding, abdominal pain, changing bowel habits and intussusception above all in children. Removal is important in order to differentiate the condition from other polyps.



Adenomas are the most frequently observed neoplasms. By definition adenomas are benign lesions but there is a relationship to the development of invasive cancer (Vogelstein 1990). There are three forms of colonic adenomas: tubular, villous, and mixed.

Tubular adenomas are the most common; about 5–10% of adenomas are tubulovillous and only 1% are villous. Adenomas arise as a result of epithelial proliferative dysplasia. Dysplasia may range from mild to severe. In all three adenoma forms carcinoma in situ (premalignant lesion) may occur. A carcinoma in situ is a preinvasive form of high grade neoplasia without light microscopic evidence of invasion through the basement membrane. The majority of invasive adenocarcinomas of the colon arises from this kind of premalignant lesions. The malignant risk with adenomatous polyps is correlated with polyp size, histologic architecture and the severity of epithelial dysplasia. The invasive form of carcinoma is rare in tubular adenomas smaller than 1 cm. The adenoma polyps are slow growing; the size doubling time is about 10 years. Severe dysplasia are frequently found in villous areas (Crawford 1994).

Tubular adenomas

Half of the tubular adenomas are found in the rectosigmoid and occur singly. Histologic examination reveals gland or cystlike structures in the submucosa (Crawford 1994).

Villous adenomas

Villous adenomas are mostly found in the rectum and sigmoid. There are generally sessile and present as a cauliflowerlike mass. The risk of cancer is high (up to 40%) in sessile villous adenomas more than 4 cm in size (Crawford 1994).

Tubulovillous adenomas

Tubulovillous adenomas show an intermediate status between the tubular and villous lesions. The risk of harboring in situ or invasive carcinoma generally correlates with the proportion of the lesion that is villous (Crawford 1994).


Rectal bleeding is the most frequent presenting complaint. Change in bowel habits and mucous discharge are much more frequent concerns in a patient with a large villous adenoma. Because of early endoscopic diagnosis nowadays hyperkalemia and dehydration are quite rare symptoms. It is attributed to the loss of fluid and electrolytes from mucous secreting tumors. Large tumors of the rectum may prolapse through the anal canal.

Diagnostics – therapy

Colonoscopy and colonoscopic polypectomy are the diagnostic and therapeutical modalities that have been responsible for the knowledge of polypoid disease in the last decades (Goodman 1998). Other means of diagnostic procedures like barium enema or double contrast, give a lower yield in identifying colonic polyps. Read prospectively analyzed small polyps (≤ 5 mm in diameter) detected by sigmoidoscopy with respect to proximal colon tumors (Read 1997). Patients with small tumors were found to have 29%, and 57% with large polyps had one or more proximal neoplasms in the colon. Total colonoscopy in individuals with rectosigmoid adenomas 5 mm or smaller is indicated.

The only adequate treatment for pedunculated or sessile adenomas is complete resection. If adenomatous epithelial remains behind the patient is still considered to have a premalignant lesion. Invasive carcinoma may already be present in the residual adenoma tumor tissue. It’s presence can not be excluded by histologic examination of the resected portion (Crawford 1994).

Mesenchymal lesions


Apart from hyperplastic polyps lipomas are the second most common benign tumor of the colon after adenomatous polyps and the most common intramural tumor. They are well differentiated arising from deposits of adipose connective tissue in the bowel wall (90% submucosal, 10% subserosal) (Corman, 1998). Most colonic lipomas are asymptomatic, they are mostly diagnosed with colonoscopy as soft yellowish tumors or polyps which are described as cushion sign identified with pressure from a biopsy forceps (Rodriguez 1990). As long as colonic lipomas are asymptomatic they do not require treatment. However with size in excess of 2 cm they give rise to some symptoms: constipation, diarrhea, abdominal pain, rectal bleeding and intussusception (Zurkirchen 1998). Colonoscopic resection is the treatment of choice. If not possible a limited segmental resection or colotomy with lipomectomy can be advised. Rectal lipomas may be insized and enucleated if confined to the rectal wall.


Benign smooth muscle tumors of the colon are extremely rare (MacKenzie 1954). The intracolonic type may be pedunculated or sessile. The tumor may be an incidental finding in asymptomatic individual. Patients sometimes present with pain, intestinal obstruction, hemorrhage or resistance in the abdomen.

The tumors tend to protrude. Leiomyomas are histologically typical spindle cell neoplasms. Most investigators believe that the mitotic rate is the single most important criterion for a diagnosis of malignancy (Berg 1960). If the mitotic rate is high, if growth is rapid, if an ulcer is present or if the lesion is > 2,5 cm in diameter, malignant degeneration should be suspected. Surgical excision results in cure unless the tumor is extraperitoneal or rectal. Smaller leiomyomas usually cause no symptoms and can be found on routine rectal examination and are usually removed with diathermia snare or by transanal excision. Recurrences are frequent, mostly due to malignant transformation (Corman 1998).


Neuroma, neurofibroma are rare histologies found in the colon and rectum. Visceral involvement in disseminated neurofibromatosis von Recklinhausen is an extremely rare appearance of the disease. Gastrointestinal bleeding or intestinal obstruction are the main symptoms. Sarcomatous degeneration is a recognized complication (Reiss 1971). The possibility of such an association is still controversial.

Treatment has been local excision, if possible or resection. For most lesions colonoscopic removal may proof to be the optimal therapy (Madiedo 1980).



It is one of the rarest tumor found in the colon (Gentry 1949). The pathogenesis is probably congenital.

Capillary hemangiomas consist of small, thinwalled, closely packed vessels with a well differentiated hyperplastic endothelial lining. They arise from submucosal vascular plexus and are often encapsulated. Ulcerations may be observed (Corman 1998).

Cavernous hemangiomas are composed of large thin vessels. They are much larger than those of capillary hemangiomas. They are usually of sufficient size to produce symptoms as obstruction and hemorrhages. They often involve 20 to 30 cm of the bowel, occasionally in multiple locations. Thrombosis is common in cavernous hemangiomas; calcification frequently occurs. The most common complication of colonic hemangiomas is bleeding (60 to 90%). Capillary hemangiomas bleed episodically, slowly and persistently. Cavernous hemangiomas tend to bleed massively.

Selective angiography may reveal a vascular malformation. Diagnosis is made by colonoscopy where the tumor will be deeply red or purple. Uncontrolled hemorrhages following colonoscopic biopsy has to be considered (Hasegawa 1981). Resection of a bleeding colonic hemangioma is the optimal treatment (Coppa 1984). The benign nature of the lesion has to be confirmed by adequate frozen section. Local excision of the hemangioma is sufficient. Hemangiomas of the rectum may be treated by sclerosing therapy, local excision or resection with coloanal anastomosis. If there is no evidence for malignant change and the hemorrhage can be controlled sphincter saving procedures should be attempted (Aylward 1988). Radiation therapy in the rectum may be an alternative approach (Hoehn 1970).


The colon is the least frequent site of a lymphangioma. This submucosal lesion is being diagnosed with increased frequency of endoscopic procedures. Lymphangiomas may be pedunculated. Lesions of this kind can be safely removed via the colonoscope (Poulos 1997). Limited resection should be considered for all sessile tumors.


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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6994


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