Colonic polyps

Last updated: September 18, 2024

Summary

Colonic polyps are abnormal colonic mucosal overgrowths. They are most common in people over 50 years of age but can also be found in younger patients who have hereditary polyposis syndromes. Affected individuals are typically asymptomatic but may present with gastrointestinal (GI) bleeding, iron deficiency anemia, and/or mechanical bowel obstruction (e.g., due to intussusception). Colonic polyps are classified macroscopically as either pedunculated (i.e., with a stalk) or sessile (i.e., without a stalk). They are classified histologically as adenomatous (most common), hyperplastic, inflammatory, serrated, or hamartomatous. Colonoscopy, which enables direct visualization biopsy and removal of the polyp, is the first-line diagnostic and therapeutic modality. Polyp removal is recommended because, although this condition is typically benign, it may transform to colorectal cancer. Adenomas (e.g., adenoma-carcinoma sequence) have the highest malignancy potential (∼ 5%). Patients with polyps that are concerning for malignancy and/or a history of familial adenomatous polyposis syndrome often require surgical resection. Regular follow-up surveillance is required following the removal of the polyps.

Epidemiology

Age
- ∼ 30% of individuals > 50 years
- Incidence increases with age.
Frequency
- ∼ 70%: adenomatous polyps
- ∼ 20%: hyperplastic polyps
- < 10%: other kinds of polyps (traditional serrated adenomas, sessile serrated adenomas, and mixed mucosal polyps)
Sex: ♂ > ♀
Race: more common in Black populations ^[1]

References: ^[2]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

The exact etiology is unknown. Risk factors include the following: ^[1]

Lifestyle
- Diet: high in red meat and fat; low in fiber and folic acid
- Obesity and lack of exercise
- Cigarette smoking
- Alcohol consumption
Genetic predisposition: hereditary polyposis syndromes

Classification

Macroscopic classification of colonic polyps

Pedunculated: attached to the GI mucosa by a stalk
Sessile: have a broad base (no stalk)

Pedunculated adenomatous polyp Tubular adenoma Villous adenoma

Histologic classification of colonic polyps

Histologic classification of colonic polyps ^[3]^[4]^[5]
Histological type	Subtypes	Characteristics	Malignant potential
Inflammatory polyps (pseudopolyps)		Seen in inflammatory bowel disease, especially ulcerative colitis, secondary to mucosal ulceration and regeneration Multiple, benign polyps	Low malignant potential
Mucosal polyps		Benign (no clinical significance) Typically small < 5 mm Mostly appear like normal mucosa
Submucosal polyps		Benign Submucosal lipoma is the most common subtype.
Hyperplastic polyps		Most common type of nonneoplastic polyp among those with low malignant potential Small (< 5 mm) Common in the distal colon (rectosigmoid) Might transform to serrated polyps Histology: hyperplasia of normal cellular components with a sawtooth/serrated pattern of crypt epithelium
Hamartomatous polyps ^[6]		May occur throughout the GIT Composed of normal tissue native to the site of origin (e.g., colon) but with disorganized growth Associated syndromes Juvenile polyposis syndrome Peutz-Jeghers syndrome Cowden syndrome Cronkhite-Canada syndrome	Low for solitary polyps Increased risk of colonic and extra-colonic malignancies when associated with syndromes
Serrated polyps	Sessile serrated polyps	Sessile lesions > 5 mm in size Common in the proximal colon (ascending colon) Morphology similar to hyperplastic polyps	Moderate malignant potential (∼ 5%) ^[7]
Serrated polyps	Traditional serrated adenoma	Common in rectosigmoid Histology: serrated architecture with dysplasia, sawtooth pattern of crypt epithelium	Moderate malignant potential (∼ 5%) ^[7]
Adenomatous polyps	Tubular adenoma	Frequency: 65–80% ^[3] Location: anywhere in the colon Histology: proliferating cells forming tubules	High malignant potential ^[3] Tubular adenoma: < 5% Tubulovillous adenoma: ∼ 20% Villous adenoma: ∼ 50%
	Tubulovillous adenoma	Frequency: 10–25% ^[3] Histology: a mixture of tubular and villous histological picture
	Villous adenoma	Frequency: 5–15% Location: common in the rectum Larger than other adenomas (cauliflower-like), and often sessile Histology: finger-like projections lined by dysplastic epithelium

The majority of colon carcinomas develop from adenomas (adenoma‑carcinoma sequence). However, only ∼ 5% of adenomas develop into colon cancers.

Villous adenomas are villains because they have the highest malignant potential.

Pseudopolyp Colonic lipoma Hyperplastic polyp Hamartomatous polyp Colonic polyps Colorectal carcinoma and adenomatous polyps Tubular adenoma Villous adenoma of the colon

Clinical features

Mostly asymptomatic
If symptomatic:
- Hematochezia (the most common symptom)
- Change in bowel habits (constipation/diarrhea)
- Mucus in stool
- Pallor
- Palpable rectal polyps on digital rectal exam
- Bowel obstruction

Subtypes and variants

Hereditary polyposis syndromes ^[8]^[9]^[10]

Consist of adenomatous polyposis syndromes and hamartomatous polyposis syndromes
Associated with:
- Increased risk of colon cancer
- Tumors in other parts of the GI tract
- Extraintestinal manifestations (e.g., tumors, cysts, cardiac conditions, pigmentation changes)
After diagnostic confirmation of hereditary polyposis syndromes, the following are recommended: ^[11]
- Referral to gastroenterology
- Surveillance for intestinal and extraintestinal malignancies
- Referral of the patient and at-risk family members for genetic counseling ^[8]

At-risk family members who decline genetic testing should undergo the same endoscopic surveillance as individuals with known mutations. ^[8]

Adenomatous polyposis syndromes ^[8]^[9]^[10]

Overview of adenomatous polyposis syndromes ^[8]^[9]^[10]
Syndrome	Characteristic features	Diagnostic findings	Management ^[9]
Familial adenomatous polyposis (FAP) ^[9]^[10]^[12]	Incidence: 1:∼7,000–30,000 births (♀=♂) ^[9] Inheritance: autosomal dominant (one-third of cases are due to de novo mutations) ^[10] Intestinal manifestations Polyps develop in the second/third decade of life but patients are usually asymptomatic until symptoms of colon cancer develop. Lifetime colorectal cancer risk: 100% (onset typically occurs at 35–40 years of age) ^[8]^[9] Increased risk of gastric and pancreatic cancer ^[10] Extraintestinal manifestations: depends on the subtype Classic FAP: none Gardner syndrome Bony and/or soft tissue tumors (e.g., osteomas of the mandible or skull, desmoid tumors) Cutaneous lesions (e.g., sebaceous cysts, lipomas, fibromas) Supernumerary and/or impacted teeth ^[13] Congenital hypertrophy of the retinal pigment epithelium: round or oval, darkly pigmented lesions on the retina Turcot syndrome (considered a variant of FAP but is also associated with Lynch syndrome): malignant brain tumors Gliomas in Lynch syndrome Medulloblastomas in FAP	Sigmoidoscopy/colonoscopy and histology > 100 adenomatous polyps throughout the colorectum Desmoid tumors Genetic testing: mutations in the tumor-suppressing APC gene (on chromosome 5q22) found in 70–90% patients ^[10]	Surveillance Flexible sigmoidoscopy (no known polyps) or colonoscopy (known polyps): every 1–2 years starting at 10–15 years of age ^[9]^[10]^[11] EGD: every 6 months–4 years starting at 25–30 years of age ^[9]^[10] Screen annually for extraintestinal complications. ^[9] Thyroid examination and ultrasound Abdominal examination for desmoid tumors Treatment Prophylactic proctocolectomy with ileoanal anastomosis or ileostomy ^[10] NSAIDs (e.g., sulindac) may reduce the polyp burden. ^[9]^[10]
Attenuated FAP	Incidence: unknown Inheritance: autosomal dominant Intestinal manifestations Delayed manifestation compared to classic FAP ^[9]^[10] Lifetime colorectal cancer risk: ∼ 70% (onset typically at ∼ 55 years of age) ^[9] Extraintestinal manifestations: none	Colonoscopy and histology 10–99 adenomatous polyps Typically located more proximally than in classic FAP ^[10] Genetic testing: mutations in the APC gene found in 70–90% patients ^[10]	Surveillance Similar to FAP Delayed onset of screening colonoscopies: every 1–2 years starting at 18–20 years of age ^[9] Treatment Similar to FAP Colon polypectomy may delay or obviate the need for preventive surgery. ^[8]
MUTYH-associated polyposis ^[10]	Incidence: unknown Inheritance: autosomal recessive Intestinal manifestations Symptoms of colonic polyps Lifetime colorectal cancer risk: 43–100% (onset typically at ∼ 50 years of age) ^[9] Extraintestinal manifestations: increased risk of ovarian, endometrial, breast, thyroid, and skin cancers ^[14]	Colonoscopy and histology: 20–99 colorectal adenomatous polyps (Hyperplastic or sessile serrated polyps are also commonly found. Duodenal polyposis frequently occurs.) ^[9]^[10] Genetic testing: mutations in the MUTYH gene (16–40% of patients) ^[10]	Surveillance Colonoscopy: every 1–2 years starting at 25–30 years of age ^[9] EGD: baseline at 30–35 years of age ^[9]^[10] Treatment Colon polypectomy Surgery referral if there are too many polyps to manage endoscopically

Colonoscopy, not sigmoidoscopy, is the first-line screening modality for individuals with attenuated FAP or MUTYH-associated polyposis because these conditions typically manifest with proximal colonic polyps. ^[8]^[9]^[10]

Counsel patients on the course of polyposis syndromes and the need for adherence to surveillance protocols. ^[8]

The Turban covers the head: Turcot syndrome is associated with malignant brain tumors. Atypical congenital hypertrophy of the retinal pigment epithelium in familial adenomatous polyposis (FAP)

Hamartomatous polyposis syndromes ^[9]^[10]

Hamartomatous polyposis syndromes ^[9]^[10]
Syndrome	Characteristic features	Diagnostic findings	Management
Peutz-Jeghers syndrome (PJS)	Incidence: 1:50,000–200,000 births ^[9] Inheritance: autosomal dominant Intestinal manifestations Large polyps can manifest with abdominal pain, GI bleeding, or intestinal obstruction. Lifetime colorectal cancer risk: ∼ 40% (onset typically occurs at ∼ 45 years of age) and increased risk of other GI malignancies (e.g., small bowel, pancreatic, stomach cancer) ^[9] Extraintestinal manifestations Mucocutaneous hyperpigmented macules (i.e., lentigines) on the lips, buccal mucosa, genitals, palms, soles (seen in 95% of patients) ^[9] Increased risk of non-GI tract cancers (e.g., breast cancer, ovarian cancer) ^[10]	Endoscopy and histology: hamartomatous PJS polyps throughout the GI tract Genetic testing : mutations in the STK11 gene on chromosome 19p13.3 (80–94% of patients) ^[9]^[10]	Surveillance Colonoscopy, EGD, and video capsule endoscopy: baseline at 8 years of age ^[9]^[10] Screen annually for associated cancers. ^[9] Treatment ^[9] Colon polypectomy Refer to surgery if there are too many polyps to manage endoscopically.
Juvenile polyposis syndrome (JPS) ^[9]	Incidence: 1:100,000–160,000 births ^[9] Inheritance: autosomal dominant with incomplete penetrance ^[9] Intestinal manifestations: can start in the first decade of life ^[9]^[10] Gastrointestinal bleeding and anemia Lifetime colorectal cancer risk: 38–68% (onset typically at 34–44 years of age) Increased risk of other GI malignancies e.g., small bowel, pancreatic, and stomach cancer ^[9]^[10] Extraintestinal manifestations Hemorrhagic telangiectasias Structural heart disease Epilepsy, macrocephaly, hydrocephalus	Endoscopy and histology: between five and hundreds of hamartomatous JPS polyps throughout the entire GI tract, predominantly in the colon ^[9] Genetic testing : mutations in the SMAD4 and BMPR1A genes (40–60% of patients) ^[9]^[10]	Surveillance ^[9]^[10] Colonoscopy and EGD: every 1–3 years starting at 12–15 years of age If SMAD4 mutation is present, perform annual: Cardiovascular exam CBC Screening and surveillance of hereditary hemorrhagic telangiectasia Treatment ^[9] Colon polypectomy Refer to surgery if there are too many polyps to manage endoscopically or there are significant symptoms of colonic polyps
Cowden syndrome (most common PTEN hamartoma tumor syndrome) ^[15]	Incidence: 1 in 200,000 births Inheritance: autosomal dominant Intestinal manifestations Often asymptomatic Possible symptoms of colonic polyps Lifetime colorectal cancer risk: 9–16% ^[9]^[10] Extraintestinal manifestations ^[16] Skin: papules and hyperkeratosis Increased risk of breast, thyroid, and endometrial tumors	Endoscopy and histology Colonic polyposis: between a few and hundreds of polyps of various types Diffuse esophageal acanthosis Genetic testing: PTEN gene mutation in 70–85% of patients	Surveillance Coloscopy and EGD: every 2 years starting at 15 years of age ^[9]^[10] Screen for associated cancers. ^[9] Treatment Colon polypectomy High rates of dysplastic polyps may necessitate colectomy. ^[17]

25% of patients with hamartomatous polyposis syndromes have no family history (i.e., de novo mutation), and ≥ 10% of patients have negative genetic testing. ^[10] Peutz-Jeghers syndrome

Nonhereditary polyposis syndromes

Serrated polyposis syndrome ^[5]^[9]^[18]

Definition: a condition in which multiple serrated polyps form in the colon; associated with an increased risk of colon cancer
Prevalence: ∼1:100,000 ^[9]^[18]
Etiology
- Unclear; smoking may be a risk factor ^[5]
- Familial association may be present; no gene has been identified ^[18]
Diagnostic findings: serrated polyps throughout the colon ^[18]
Management ^[9]
- Surveillance colonoscopy every 1–3 years with polypectomy of all polyps > 5 mm ^[9]
- Surgery (colectomy with ileorectal anastomosis) may be required if there are too many polyps to manage endoscopically.

Cronkhite-Canada syndrome ^[19]^[20]

Definition: an extremely rare form of nonhereditary hamartomatous polyposis; associated with an increased risk of colorectal cancer ^[19]
Etiology: unclear; likely immune-mediated
Clinical features: typically manifests in individuals ∼ 60 years of age ^[19]
- Symptoms of colonic polyps, including gastrointestinal hemorrhage
- Protein-losing enteropathy
- Extraintestinal manifestations ^[21]
  - Ectodermal changes
  - Sepsis
  - Congestive heart failure
Diagnostic findings: numerous hamartomatous polyps; inflammatory changes within polyps
Management
- Nutritional support for protein loss from chronic diarrhea
- Consider immune suppression with glucocorticoids or azathioprine.
- Cancer screening: optimal intervals unclear, colonoscopy usually performed annually ^[20]

Management

Approach

Request for all patients with suspected polyps (e.g., positive family history, symptoms of colonic polyps):
- CBC for anemia
- Colonoscopy with polypectomy/biopsy
  - Confirmatory test
  - Alternatives include flexible sigmoidoscopy, CT colonoscopy, and double-contrast barium enema ^[22]^[23]
Send any samples for histologic classification of colonic polyps.
- No concerning features: Further treatment is not required.
- Malignant features: Treat as colorectal cancer.
- Features of hereditary polyposis syndromes: Refer to gastroenterology and genetics. ^[9]^[10]
Follow-up is required for all patients because of the increased risk of malignancy.

Polyps are often identified as an incidental finding on workup for other conditions.

Patients with red flags for colon cancer or positive colorectal cancer screening tests (e.g., fecal occult blood testing) should undergo diagnostics for colorectal cancer.

Colonoscopy ^[24]^[25]

Colonoscopy facilitates simultaneous diagnosis and management of most polyps; suspected malignant colorectal polyps should be biopsied and referred to surgery.

No polyps present
- No hereditary polyposis syndrome: Consider differential diagnostics.
- Hereditary polyposis syndrome: Arrange surveillance colonoscopy.
Polyps present
- Stratify risk to determine if polypectomy or biopsy is appropriate.
- Advanced endoscopy techniques (e.g., chromoendoscopy, narrow-band imaging) may be required to identify high-risk features.

Recommended removal techniques for low and high-risk colonic polyps ^[24]^[26]^[27]
Suspected polyp type	Characteristic features	Recommended excision technique
Low-risk	Sessile and < 10 mm Pedunculated at any size	Lesions of either type (< 10 mm): cold snare polypectomy Pedunculated lesions ≥ 10 mm: hot snare polypectomy
High-risk	Sessile and ≥ 10 mm Dominant nodule Ulceration No lifting with submucosal injection	Lesion with no evidence of deep mucosal invasion 10–20 mm: hot or cold snare polypectomy ≥ 20 mm: endoscopic mural resection Evidence of submucosal invasion: biopsy and refer to surgery

Patients with hereditary polyposis syndromes with multiple polyps that cannot be managed endoscopically should also be referred for surgery.

Endoscopic colon polypectomy ^[24]^[25]

Techniques

Snare polypectomy
- A thin wire snare encircles the polyp including a surrounding margin of healthy tissue.
- The snare is then retracted, which causes it to tighten and cut through the encircled tissue.
- Can be performed with electrocautery (i.e., hot snare) or without (i.e., cold snare)
Endoscopic mucosal resection
- The submucosa under the polyp is injected to lift the polyp away from the deeper mucosa.
- A snare procedure is then performed to excise the polyp.

Hot snare polypectomy

Complications ^[24]^[25]^[28]

Postpolypectomy bleeding: lower gastrointestinal bleeding that occurs up to 30 days postpolypectomy ^[24]
- Risk factors include: ^[24]
  - Patient: anticoagulant use, chronic renal disease, cardiovascular disease
  - Lesion: size ≥ 10 mm, located in ascending colon, pedunculated with thick stalk
- Management
  - Intraprocedural bleeding: See “Endoscopic hemostasis.”
  - Postprocedural bleeding
    - Stabilize patients with hemorrhagic shock.
    - Consult gastroenterology urgently. ^[28]^[29]
    - See “Management of GI bleeding.”
- Prophylactic measures
  - Periprocedural management of oral anticoagulant therapy for patients on anticoagulants
  - Ligation of pedunculated polyps ≥ 20 mm prior to removal
  - Injection of a vasoconstrictor (e.g., epinephrine) ^[24]
Bowel perforation
Postpolypectomy coagulation syndrome
- Thermal injury to the bowel wall causes inflammation that leads to fever, localized abdominal pain, and elevated WBC count.
- Normally self-limiting with supportive treatment (e.g., fluids, antibiotics, bowel rest)

Surgical resection ^[24]^[25]^[30]

Colon resection may be required for suspected ; or confirmed malignancy (see “Surgery for colorectal cancer”).
Hereditary polyposis syndromes may require ; surgical polyp removal (e.g., for large polyps) and/or colonic resection.

Refer patients with low-risk polyps that are difficult to remove (e.g., due to size and/or location) to an endoscopist with experience in advanced endoscopic removal techniques prior to referring to surgery. ^[24]

Follow-up ^[31]^[32]

The guidance in this section is for patients with no additional risk factors. For individuals at high risk of CRC, follow colorectal cancer screening in high-risk individuals. For individuals with hereditary polyposis syndromes, follow condition-specific screening procedures (see “Subtypes and variants”).

Surveillance after colon polypectomy ^[31]^[32]
Risk category	Recommended interval to repeat colonoscopy
Very low risk	10 years
Low-risk	7–10 years
Intermediate risk	3–5 years
High-risk	3 years
Very high risk: > 10 adenomas	1 year ^[9]

Follow-up should be tailored to the histology of the colonic polyp and the patient's risk factors for colorectal cancer.

Related One-Minute Telegram

One-Minute Telegram 68-2023-3/3: They tested their poo, but didn’t follow through
One-Minute Telegram 62-2022-3/3: Colonoscopy for colorectal cancer screening saves lives, but only if you get one

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

Start your trial, and get 5 days of unlimited access to over 1,100 medical articles and 5,000 USMLE and NBME exam-style questions.

Start free trial

Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer