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Colorectal polyps are mucosal growths that protrude into the lumen of the colon or rectum and vary in histologic type, morphology, and malignant potential. Histologic categories include hyperplastic, inflammatory, hamartomatous, and neoplastic lesions. Macroscopic classification reflects morphology, with sessile polyps arising directly from the mucosa and pedunculated polyps attached by a fibrovascular stalk. Neoplastic polyps, particularly adenomas, hold the greatest clinical importance because of their potential for malignant transformation and their role as precursors to most colorectal cancers. Incidence increases with age, making screening and surveillance essential for early detection and prevention. Colonoscopy enables direct visualization, biopsy, and removal of polyps, representing a critical strategy for interrupting progression from adenoma to carcinoma. This educational activity strengthens the clinician’s ability to evaluate and manage colorectal polyps through a comprehensive review of etiopathogenesis, classification systems, diagnostic methods, and evidence-based management strategies. Participants gain insight into risk factors, screening recommendations, and the identification of hereditary polyposis syndromes such as familial adenomatous polyposis, Lynch syndrome, juvenile polyposis, and Peutz-Jeghers syndrome. Emphasis on collaboration with gastroenterologists, surgeons, pathologists, genetic counselors, nurses, and other interprofessional team members highlights coordinated screening, accurate diagnosis, genetic risk assessment, and appropriate surveillance, which together improve early detection and enhance patient outcomes. Objectives: Differentiate benign from malignant colorectal polyps using clinical, endoscopic, and histopathologic criteria. Create evidence-based, patient-specific management plans for colonic polyps, integrating treatment, surveillance, and strategies to prevent malignant transformation. Improve patient awareness regarding the detection, management, and prevention of complications associated with colonic polyps. Collaborate with all members of the interprofessional healthcare team, including specialists such as gastroenterologists, colorectal surgeons, radiologists, and medical geneticists, to provide efficient, comprehensive, and coordinated care for patients with colorectal polyps and polyposis syndromes.

Improve patient awareness regarding the detection, management, and prevention of complications associated with colonic polyps. Collaborate with all members of the interprofessional healthcare team, including specialists such as gastroenterologists, colorectal surgeons, radiologists, and medical geneticists, to provide efficient, comprehensive, and coordinated care for patients with colorectal polyps and polyposis syndromes. Access free multiple choice questions on this topic.

A polyp is a mass protruding into the lumen of a viscus. Colorectal polyps arise in the large intestine and occur as isolated lesions or part of polyposis syndromes. Size-based classification defines polyps as diminutive (<6 mm), small (6–9 mm), or large (>9 mm). Morphologically, these growths are either sessile, presenting flat along the mucosal surface, or pedunculated, featuring a fibrovascular stalk. Histological classification remains the primary determinant of clinical significance, comprising hyperplastic, inflammatory, and neoplastic polyps.[1] Neoplastic or adenomatous polyps possess the greatest malignant potential and account for most colorectal cancers (CRCs).[2] Serrated polyps also contribute to the adenoma–carcinoma sequence, representing 15% to 30% of CRC cases.[3] Hyperplastic and inflammatory polyps typically present in younger patients and carry low malignant potential. Polyposis denotes a systemic process leading to multiple gastrointestinal polyps. Most cases are hereditary, representing 1% to 7% of CRCs, and may include extracolonic manifestations. Early detection, rigorous surveillance, and timely interventions are essential to prevent malignancy. Specific polyposis syndromes differ in genetic alterations, clinical features, polyp morphology and distribution, and associated cancer risk.[4]

Multiple and, sometimes, uncertain factors contribute to the development of colorectal polyps. Neoplastic polyps arise from a combination of genetic predisposition and environmental influences. Smoking increases the risk of colorectal polyps.[5] Additional risk factors include obesity, high red meat consumption, and low intake of fiber and calcium.[6] Use of nonsteroidal anti-inflammatory drugs and statins demonstrates a protective effect against polyp formation.[7] Serrated adenomas are associated with microsatellite instability, particularly hypermethylation of the MLH1 gene and mutations of the BRAF gene.[8] Hamartomatous polyps occur either as solitary growths or part of polyposis syndromes, including Peutz-Jeghers (PJS), Cowden, and juvenile polyposis (JPS) syndromes.[9] Inflammatory polyps, also called "pseudopolyps," develop in patients with inflammatory bowel disease (IBD), most commonly ulcerative colitis. Polyp formation can also follow episodes of infectious or ischemic colitis.[10] Dysregulated intestinal microbiota and chronic inflammation represent additional risk factors for colorectal polyps.[11] Polyposis syndromes are hereditary disorders caused by various genetic mutations. Familial adenomatous polyposis (FAP) is an autosomal dominant condition resulting from a mutation in the APC gene on chromosome 5q.[12] MUTYH-associated polyposis (MAP) is an autosomal recessive syndrome caused by biallelic mutations in the MUTYH gene, which is responsible for base excision repair.[13] PJS is an autosomal dominant disorder caused by a mutation of the STK11 gene on chromosome 19p.[14] Familial juvenile polyposis results from mutations in the tumor suppressor gene SMAD4 on chromosome 10q.[15] PTEN hamartomatous tumor syndromes, including Cowden and Bannayan-Riley-Ruvalcaba syndromes, are autosomal dominant disorders caused by abnormalities in the PTEN gene on chromosome 10q.[16] Hereditary mixed polyposis syndrome follows an autosomal dominant inheritance pattern due to abnormalities in the SMAD4 and BMPR1A genes.[17] Cronkhite-Canada syndrome is a rare, acquired, nonfamilial disorder characterized by gastrointestinal polyposis of unknown etiology.[18]

Hyperplastic polyps represent the most common histological variant of colorectal polyps. The incidence of colorectal polyps, particularly adenomatous types, increases with advancing age and is higher in men. In the United States, adenomatous polyps are detected in 20% to 40% of screening colonoscopies in adults older than 50. Among younger adults, the incidence is approximately 12% in women and 24% in men. The incidence rises to 27% in women and 40% in men in adults older than 80.[19] Detection of colorectal polyps in asymptomatic individuals reaches 34.3%, with up to 50% presenting synchronous lesions.[20][21] In children, the incidence ranges from 4% to 12%, with most cases involving hamartomatous polyps.[22] The prevalence of colorectal polyps is higher among non-Caucasian populations.[23]

Spontaneous somatic mutations in the APC gene of colonic epithelial cells are postulated to initiate adenomatous polyp development. These mutations occur early in adenoma formation and are detectable in aberrant crypts. Adenomas remain benign for years until additional genetic alterations drive malignant transformation. Transition from intermediate to late adenoma is attributed to loss of the normal DCC (deleted in colon cancer) gene, which encodes a neural cell adhesion molecule receptor responsible for apoptosis and tumor suppression. Mutation of the TP53 gene, essential for DNA repair, facilitates the progression of late adenoma into invasive carcinoma. Mutation of the KRAS oncogene promotes unregulated colonocyte replication, resulting in exophytic adenoma growth and malignant transformation in up to 50% of colon cancers.[24] Other genes implicated in CRC via the adenoma–carcinoma sequence include DNA mismatch repair genes MLH1, MSH2, and MSH6.[25] Serrated adenomas develop through hypermethylation of the MLH1 gene, a mechanism similar to sporadic microsatellite unstable cancers. Traditional serrated adenomas (TSAs) frequently exhibit BRAF mutations and hypermethylation of multiple genes known as the CpG island methylator phenotype (CIMP).[26] In hereditary CRC syndromes, loss of an allele constitutes a genetic abnormality, predisposing individuals to invasive malignancy at a younger age.[27]

Histological classification of colorectal polyps distinguishes lesions according to malignant potential. Polyps with significant malignant propensity include neoplastic or adenomatous types, which comprise tubular, tubulovillous, and villous adenomas. Serrated polyps also carry malignant risk and include TSAs and sessile serrated adenomas. Hyperplastic, inflammatory, and hamartomatous polyps have low malignant potential. Adenomatous polyps are characterized by marked complex glandular crowding, irregular architecture, cribriform patterns, and intraluminal necrosis. Cellular features include loss of polarity, enlarged nuclei with prominent nucleoli, dispersed chromatin, and atypical mitoses.[28] Tubular adenomas are frequently pedunculated and display branched tubular glands with relatively low cellular atypia. This subtype is the most common histological form of neoplastic polyps, comprising 65% to 80% of cases. Villous adenomas are often sessile and exhibit finger-like projections (see Image. Villous Adenoma). These growths constitute 5% to 10% of neoplastic polyps and frequently demonstrate severe atypia or dysplasia. Tubulovillous adenomas, representing approximately 10% to 25% of polyps, contain both tubular and villous elements. Dysplasia in adenomatous polyps varies in degree, and higher grades of dysplasia correlate with increased malignancy risk.[29] The Haggitt classification describes the depth of invasion in pedunculated malignant polyps, providing prognostic information and guiding treatment strategies.[30] This scheme classifies lesions as follows: Haggitt level 0: Limited to the mucosa Haggitt level 1: Invasion into the submucosa, limited to the head of the polyp Haggitt level 2: Invasion into the neck of the polyp Haggitt level 3: Invasion into the stalk of the polyp Haggitt level 4: Invasion into the submucosa below the level of the stalk, but above the muscularis propria

Haggitt level 0: Limited to the mucosa Haggitt level 1: Invasion into the submucosa, limited to the head of the polyp Haggitt level 2: Invasion into the neck of the polyp Haggitt level 3: Invasion into the stalk of the polyp Haggitt level 4: Invasion into the submucosa below the level of the stalk, but above the muscularis propria Serrated lesions are defined by prominent serrations, architectural distortion, and either asymmetrical proliferation, dilatation of the crypt base, or serrations extending into the crypt base. Around 2% to 5% of sessile serrated lesions exhibit dysplasia, characterized by an abrupt transition between normal and dysplastic areas. Architectural changes include villous histology, crypt elongation, crowding, complex branching, cribriform patterns, and either excessive or reduced luminal serration.[31] TSAs display a protruberant villiform growth pattern with pseudostratified columnar cells, ectopic crypt foci, and goblet cells.[32] Hyperplastic polyps are considered a subgroup of serrated polyps but carry significantly lower malignant potential. These growths exhibit cellular hyperplasia without dysplasia (see Image. Hyperplastic Polyp of the Colon). Hamartomatous or juvenile polyps contain connective tissue, including smooth muscle, lamina propria, and inflammatory infiltrates, and are covered by hypertrophic epithelium. Macroscopically, these masses resemble adenomatous polyps, often appearing pedunculated and cherry-red. Inflammatory polyps, also called "pseudopolyps," are not true polyps. These growths represent accumulations of inflammatory tissue and distorted mucosal architecture. Histologically, inflammatory polyps contain islands of normal, regenerating mucosa surrounded by areas of tissue loss.

Most colorectal polyps, including those associated with polyposis syndromes, remain asymptomatic and are incidentally detected during screening colonoscopies. Focused history should target atypical symptoms, including abdominal discomfort, occasional rectal bleeding, passage of mucus in stools, constipation, diarrhea, or a sensation of incomplete evacuation.[33] Significant symptoms may arise if large colorectal polyps cause intestinal obstruction, presenting as abdominal pain, distention, constipation, obstipation, and feculent vomiting. Chronic anemia may develop in cases of occult bleeding, and, rarely, hemorrhagic shock can result from profuse, continued bleeding from a polyp. A thorough family history is critical when evaluating patients with suspected colorectal polyps, particularly in polyposis syndromes. Since most CRC cases develop from polyps, patients with a significant family history require assessment for hereditary cancer syndromes, including Lynch syndrome and FAP. Patients with FAP may present with extracolonic manifestations, including desmoid tumors, mandibular or skeletal osteomas, retinal spots, thyroid nodules, and epidermoid cysts on the face or scalp. Lynch syndrome is associated with increased risk for CRC and cancers of the endometrium, ovary, stomach, small bowel, urinary tract, biliary tract, brain (usually glioblastoma), skin (sebaceous adenomas, sebaceous carcinomas, and keratoacanthomas), pancreas, and prostate.[34] Juvenile or hamartomatous polyposis syndromes can present with mucosal hyperpigmentation, as observed in PJS, or with anemia, rectal bleeding, or rectal prolapse, as seen in JPS. Hamartomatous polyps in both syndromes can lead to intussusception, which may cause an acute abdomen.[35] McKittrick-Wheelock syndrome occurs in patients with hypersecreting rectal polyps, presenting with severe dehydration, oliguria, or renal failure. Laboratory findings typically include hypokalemia, hyponatremia, and abnormalities consistent with uremia.[36]

Juvenile or hamartomatous polyposis syndromes can present with mucosal hyperpigmentation, as observed in PJS, or with anemia, rectal bleeding, or rectal prolapse, as seen in JPS. Hamartomatous polyps in both syndromes can lead to intussusception, which may cause an acute abdomen.[35] McKittrick-Wheelock syndrome occurs in patients with hypersecreting rectal polyps, presenting with severe dehydration, oliguria, or renal failure. Laboratory findings typically include hypokalemia, hyponatremia, and abnormalities consistent with uremia.[36] Physical examination should be comprehensive, head to toe, particularly in patients with suspected polyposis syndromes. Cutaneous swellings, hyperpigmentation of oral or tongue mucosa, absent or supernumerary teeth, mandibular swellings, abdominal wall desmoid tumors, and skeletal abnormalities warrant careful assessment. Features of advanced CRC, including cachexia, pallor, left supraclavicular lymphadenopathy, and phlebitis migrans, should also be evaluated.[37] Abdominal examination is frequently unremarkable but remains essential in patients presenting with signs of intestinal obstruction. Digital rectal examination aids in evaluating anorectal polyps and detecting evidence of hematochezia.

A comprehensive evaluation of colorectal polyps integrates laboratory analysis, stool testing, colonoscopy, and imaging. This approach enables clinicians to identify polyps, characterize their clinical significance, and determine management strategies. Initial evaluation of colorectal polyps includes blood investigations, stool assays, and, when indicated, tumor markers. Complete blood counts assess for anemia associated with chronic bleeding, while serum creatinine and electrolyte measurements are indicated in patients with hypersecretory adenomas. Carcinoembryonic antigen should be measured when malignant polyps are suspected. Stool assays detect occult bleeding from colorectal polyps. Fecal occult blood testing demonstrates limited sensitivity for small polyps, which often do not bleed. Polyps that are large (>2 cm) or progress to malignant transformation are more likely to yield positive results.[38] Fecal immunochemical testing employs antibodies specific to the globin component of hemoglobin and demonstrates higher sensitivity than traditional fecal occult blood testing. Although fecal immunochemical testing is equivalent to colonoscopy for CRC screening, its effectiveness in detecting advanced polyps is inferior.[39] Colonoscopy is the gold standard for the detection of colorectal polyps, although sensitivity is not 100% (see Image. Colonic Polyps on Colonoscopy).[40] Adenoma detection rates and missed polyp rates serve as measures of colonoscopy accuracy. Studies report an overall missed polyp rate of 22%, with higher rates for diminutive polyps.[41] Guidelines recommend routine screening colonoscopy beginning at age 40 to 50 years in average-risk patients and earlier in those at high risk.[42] High-risk conditions include FAP, where screening should begin at age 10 to 15 years, and Lynch syndrome, where colonoscopy is advised from age 24 to 35 years at intervals of 1 to 3 years (see Image. Diffuse Colonic Polyposis on Sigmoidoscopy).[43] The Paris classification categorizes colorectal polyps based on morphology and surface features.[44] This system, outlined below, aids in endoscopic assessment, risk stratification, and planning of appropriate intervention. Lesions classified as Is, IIa, IIb, or IIc may be considered laterally spreading. Such lesions typically measure more than 10 mm. I. Protruding types Ip: Pedunculated Is: Sessile

The Paris classification categorizes colorectal polyps based on morphology and surface features.[44] This system, outlined below, aids in endoscopic assessment, risk stratification, and planning of appropriate intervention. Lesions classified as Is, IIa, IIb, or IIc may be considered laterally spreading. Such lesions typically measure more than 10 mm. I. Protruding types Ip: Pedunculated Is: Sessile II. Nonprotruding and nonexcavated types IIa: Slightly elevated IIb: Completely flat IIc: Slightly depressed III. Excavated type Image-enhanced colonoscopy options include spectroscopy using near-infrared autofluorescence and narrow-band imaging. These modalities serve as adjuncts to routine white-light colonoscopy, improving the prediction of polyp pathology and increasing sensitivity and specificity to 80% and 90%, respectively.[45] Recent advances in endoscopic technology include endocytoscopy and artificial intelligence, which are anticipated to provide significant improvements in the detection and characterization of colorectal polyps.[46] Computed tomographic (CT) colonography, also known as virtual colonoscopy, uses CT of a prepared colon distended with air to generate a 3-dimensional view of the colonic anatomy. This modality is useful in patients who refuse conventional colonoscopy or have contraindications to invasive procedures. CT colonography demonstrates a sensitivity greater than 90% for detecting polyps larger than 5 mm but requires interpretation by experienced radiologists.[47] The primary limitation of this technology is its inability to perform a biopsy or polypectomy, necessitating a subsequent colonoscopy if polyps are identified. CT colonography is not recommended for patients at high risk for CRC, including individuals who have FAP or Lynch syndrome, are under surveillance for irritable bowel disease, or experience active colitis. Absolute contraindications include intestinal obstruction and recent polypectomy.[48]

The primary limitation of this technology is its inability to perform a biopsy or polypectomy, necessitating a subsequent colonoscopy if polyps are identified. CT colonography is not recommended for patients at high risk for CRC, including individuals who have FAP or Lynch syndrome, are under surveillance for irritable bowel disease, or experience active colitis. Absolute contraindications include intestinal obstruction and recent polypectomy.[48] Magnetic resonance colonography demonstrates lower accuracy compared to CT colonography. However, this imaging technique is suitable for patients with contraindications to CT, such as renal failure. Sensitivity exceeds 88% for detecting polyps larger than 10 mm.[49] Capsule endoscopy is primarily employed for the evaluation of small bowel pathology, including Crohn disease and small intestinal bleeding. Sensitivity and specificity for detecting colorectal polyps are substantially lower than those of colonoscopy, and the modality is not recommended for colorectal polyp evaluation.[50] Fecal DNA and antigen testing measures markers such as KRAS mutation, methylated BMP3, NDRG4, and β-actin, and is well established for CRC screening. Sensitivity for advanced adenomas is limited to 57%, and detection of high-grade dysplasia reaches 83%.[51][52]

Colonoscopic Polypectomy Polypectomy is the most definitive treatment for colorectal polyps and may be performed at the time of detection during colonoscopy. Recommendations for polypectomy depend on polyp size, morphology, and number. Pedunculated polyps are generally removable with standard colonoscopic tools, whereas sessile polyps pose greater technical challenges. Polypectomy should be attempted whenever polyps are identified during colonoscopy. Diminutive polyps (<6 mm) detected on CT colonography do not require excision and may be monitored with serial follow-up.[53] Polyps larger than 6 mm should be excised and submitted for histopathological examination. Multiple colonoscopic techniques exist for the removal of colorectal polyps. The selection of an appropriate method depends on polyp characteristics and anticipated procedural risk. Biopsy forceps polypectomy is indicated for the removal of small colorectal polyps. The procedure involves grasping the polyp with the forceps and retrieving the specimen with the same instrument. Biopsy forceps polypectomy is typically performed for polyps measuring less than 3 mm using standard biopsy forceps. Polyps up to 6 mm in size may be excised using large cup or jumbo forceps to ensure complete tissue retrieval. Additional bites may be taken to obtain more tissue if necessary. Cold snare polypectomy is indicated for pedunculated polyps with a size larger than 20 mm or a stalk length exceeding 5 mm. This technique is also employed for nonpedunculated polyps measuring 6 to 9 mm or 10 to 19 mm. The procedure involves encircling the polyp and a 1- to 2-mm margin of surrounding mucosa, then grasping and resecting the tissue with a snare without electrocautery. The resected specimen is then suctioned through the colonoscope.

Cold snare polypectomy is indicated for pedunculated polyps with a size larger than 20 mm or a stalk length exceeding 5 mm. This technique is also employed for nonpedunculated polyps measuring 6 to 9 mm or 10 to 19 mm. The procedure involves encircling the polyp and a 1- to 2-mm margin of surrounding mucosa, then grasping and resecting the tissue with a snare without electrocautery. The resected specimen is then suctioned through the colonoscope. Hot snare polypectomy is indicated for pedunculated polyps smaller than 20 mm with a stalk shorter than 5 mm, as well as for nonpedunculated, noninvasive lesions of intermediate size measuring 10 to 19 mm. The procedure entails encircling the polyp with a snare, slowly closing the loop to capture a 1- to 2-mm margin of normal tissue, and resecting the lesion using electrocautery. Endoscopic mucosal resection (EMR) is indicated for nonpedunculated, noninvasive lesions larger than 20 mm. The procedure involves injecting a solution into the submucosal space to elevate the lesion, followed by snare resection using a high-frequency current. Endoscopic submucosal dissection (ESD) is employed for nonpedunculated lesions with suspected superficial submucosal invasion. A 3- to 5-mm margin around the lesion is marked, and the submucosal space is injected. The circumference of the lesion is incised using an endoscopic knife with electrocautery, followed by careful submucosal dissection.[54] Complications of polypectomy include bleeding, which is generally minor for diminutive polyps but occurs more frequently with EMR and ESD. Bowel perforation may develop in up to 1.5% of patients undergoing EMR and up to 10% of those undergoing ESD, most cases being manageable endoscopically. Postpolypectomy coagulation syndrome is a rare manifestation of peritoneal irritation from electrocautery, occurring in 1.3% to 3.7% of patients. Rarely, EMR and ESD can lead to colonic stricture.[55] Surgical Interventions

Complications of polypectomy include bleeding, which is generally minor for diminutive polyps but occurs more frequently with EMR and ESD. Bowel perforation may develop in up to 1.5% of patients undergoing EMR and up to 10% of those undergoing ESD, most cases being manageable endoscopically. Postpolypectomy coagulation syndrome is a rare manifestation of peritoneal irritation from electrocautery, occurring in 1.3% to 3.7% of patients. Rarely, EMR and ESD can lead to colonic stricture.[55] Surgical Interventions Indications for surgical resection include sessile polyps that cannot be completely excised by colonoscopy and pedunculated polyps harboring invasive carcinoma extending into the stalk. Additional indications include polyposis syndromes, such as FAP requiring prophylactic proctocolectomy, and symptomatic hamartomatous polyposis.[56] Colectomy is also warranted in patients with irretrievable polyps during colonoscopy, as the incidence of cancer in this group can reach 17.7%.[57] Surgery for colorectal polyps should follow oncological principles unless a benign etiology is confirmed. These principles include complete mesocolic excision or total mesorectal excision (TME) with central vascular ligation and lymphadenectomy. Surgical options for FAP include total colectomy with ileorectal anastomosis or total proctocolectomy with ileal pouch-anal anastomosis. Total colectomy carries lower morbidity related to pelvic dissection, such as reduced risk of sexual and urologic dysfunction, but has a risk of disease recurrence in the residual rectum. Regular proctoscopic surveillance is required, with proctectomy indicated if recurrence occurs. Proctocolectomy with ileal pouch-anal anastomosis removes the entire colon and rectum, providing a permanent cure, but carries a significant complication rate, including anastomotic leak, pouch-vaginal or pouch-vesical fistula, pouchitis, incontinence, and urological or sexual dysfunction.

Surgical options for FAP include total colectomy with ileorectal anastomosis or total proctocolectomy with ileal pouch-anal anastomosis. Total colectomy carries lower morbidity related to pelvic dissection, such as reduced risk of sexual and urologic dysfunction, but has a risk of disease recurrence in the residual rectum. Regular proctoscopic surveillance is required, with proctectomy indicated if recurrence occurs. Proctocolectomy with ileal pouch-anal anastomosis removes the entire colon and rectum, providing a permanent cure, but carries a significant complication rate, including anastomotic leak, pouch-vaginal or pouch-vesical fistula, pouchitis, incontinence, and urological or sexual dysfunction. For rectal polyps, minimally invasive modalities include transanal excision (TAE), transanal minimally invasive surgery (TAMIS), and transanal endoscopic microsurgery (TEM). Indications include large benign polyps and early malignant polyps with superficial submucosal invasion (SM1 or SM2), well to moderately differentiated, and without lymph node metastasis.[58] High-resolution pelvic magnetic resonance imaging is essential for local staging of malignant polyps and assessment of high-risk features, including tumor deposits, extramural vascular invasion (EMVI), and lymphadenopathy, along with metastatic evaluation using contrast-enhanced computed tomography of the thorax and abdomen. Interprofessional team discussion is recommended before surgical planning. TAE is indicated for polyps with a diameter smaller than 4 cm, location within 8 cm of the anal verge, and a depth of invasion less than T1. With the patient in the lithotomy position, anal retractors are used to expose the polyp, and distal traction sutures are applied for retraction. A circumferential incision is made with a 1-cm margin, followed by full-thickness excision of the lesion. The resulting defect may be closed or left open. TAMIS is indicated for benign polyps and T1 cancers as curative treatment, as well as advanced cancers as a palliative option when radical resection is not feasible. Polyps located in any quadrant of the rectum may be excised. A single-port device is introduced into the anal canal with continuous carbon dioxide insufflation. Dissection is performed using conventional laparoscopic instruments, and the resulting defect may be sutured or left open.

TAMIS is indicated for benign polyps and T1 cancers as curative treatment, as well as advanced cancers as a palliative option when radical resection is not feasible. Polyps located in any quadrant of the rectum may be excised. A single-port device is introduced into the anal canal with continuous carbon dioxide insufflation. Dissection is performed using conventional laparoscopic instruments, and the resulting defect may be sutured or left open. TEM is indicated for polyps in the middle and upper rectum, as well as the rectosigmoid, up to 20 cm from the anal verge. The procedure is especially suited for polyps positioned at the 12 and 6 o’clock locations. An operating proctoscope is inserted into the anal canal, and an air seal is maintained with continuous carbon dioxide insufflation. The polyp is dissected and removed using instruments passed through the proctoscope ports.[59] Complications of transanal procedures for rectal polyps include urinary retention, urinary tract infection, bleeding, perianal abscess, and transient fecal incontinence. TAMIS and TAE may also cause bowel perforation, pelvic abscess, rectal stenosis, and rectovaginal or rectovesical fistula.

Differential diagnoses for colorectal polyps encompass both hereditary syndromes and sporadic conditions. Accurate identification is essential for appropriate management and cancer risk assessment. Hereditary colorectal polyposis syndromes comprise several distinct genetic disorders. FAP presents in classical and attenuated forms. Classical FAP is characterized by early onset and development of more than 100 adenomas throughout the colon and rectum, often accompanied by extraintestinal manifestations. Attenuated FAP manifests with 10 to 100 adenomas. MAP is defined by more than 20 adenomas, with onset typically occurring between the fourth and seventh decades of life. Lynch syndrome features 0 to 30 adenomas in the colon and rectum and carries an increased risk of stomach, urothelial, and endometrial cancers.[60] The diagnosis of PJS requires at least 2 histologically confirmed polyps, perioral pigmentation, and a supportive family history. JPS includes multiple juvenile polyps throughout the gastrointestinal tract or more than 5 polyps in the colorectum. Cowden syndrome is characterized by multiple polyps in the stomach, small intestine, and colon, with associated risks of mucocutaneous tumors and cancers of the breast, endometrium, and thyroid, and other hamartomatous lesions.[61] Sporadic colorectal lesions encompass a variety of acquired and nonhereditary conditions. Inflammatory polyps are associated with irritable bowel disease and infectious colitis. Hyperplastic polyps are defined by the presence of at least 5 histologically confirmed lesions proximal to the sigmoid colon, with at least 2 exceeding 1 cm in size.[62] Hereditary mixed polyposis syndrome is characterized by a mixture of different polyp types.[63] Cronkhite-Canada syndrome presents with hamartomatous polyps throughout the gastrointestinal tract, sparing the esophagus. Ganglioneuromatous polyposis consists of hamartomatous polyps occurring synchronously with adenomas and juvenile polyps.[64] Intestinal leiomyomatosis is defined by the proliferation of smooth muscle cells and hyalinization of vessel walls.[65] Pneumatosis cystoides intestinalis manifests as sessile pseudopolyps in the submucosa or subserosa, most commonly in the terminal ileum, with characteristic imaging findings such as intramural gas, ascites, and portal venous air.[66]

Intestinal leiomyomatosis is defined by the proliferation of smooth muscle cells and hyalinization of vessel walls.[65] Pneumatosis cystoides intestinalis manifests as sessile pseudopolyps in the submucosa or subserosa, most commonly in the terminal ileum, with characteristic imaging findings such as intramural gas, ascites, and portal venous air.[66] Nonpolypoid submucosal lesions include lipomas, gastrointestinal stromal tumors, neuroendocrine tumors, and hemorrhoids.

Colorectal polyps are frequently identified on screening colonoscopies and are predominantly benign. A subset of these lesions is neoplastic, carrying malignant potential and requiring intervention. Early detection and removal of neoplastic polyps represent an effective strategy for preventing progression to CRC and associated morbidity. Polyposis syndromes necessitate molecular and genetic testing to confirm the diagnosis and require regular surveillance with colonoscopy. FAP carries a near-absolute risk of CRC by the fourth decade, mandating prophylactic proctocolectomy. Patients with Lynch syndrome and MAP also require structured screening and appropriate management. The prognosis of colorectal polyps is determined by histologic type, number, and underlying etiology.

Most colorectal polyps remain asymptomatic and are detected only when complications arise, such as bleeding, intestinal obstruction, altered bowel habits, secretory diarrhea with dyselectrolytemia, and progression to invasive carcinoma. Low rectal polyps can lead to rectal prolapse, ulceration, and secondary infection.

Colorectal polyps, particularly neoplastic types, carry a significant risk due to potential transformation into malignant neoplasms. Most CRC cases arise from precursor polyps, making early identification and treatment essential for prevention. Patient education on etiology and risk factors is critical. Modifiable factors, including smoking and high intake of alcohol and red meat, should be addressed. Screening colonoscopies play a central role in both the diagnosis and management of colorectal polyps. Individuals at average risk should begin screening at age 40 years, as recommended by primary physicians. Patients with known colorectal polyps should be informed about high-risk symptoms, including rectal bleeding, intestinal obstruction, altered bowel habits, and secretory diarrhea. Hereditary polyposis syndromes, such as FAP, Lynch syndrome, JPS, and PJS, require early screening and regular follow-up. Family members of affected individuals should also undergo appropriate surveillance. Prophylactic proctocolectomy is indicated for individuals with FAP who carry a near-absolute risk of CRC if left untreated.

Dietary and lifestyle modifications may reduce the incidence of colorectal polyps. Recommended measures include maintenance of a low-fat, high-fiber diet, reduced alcohol consumption, and smoking cessation. No reduction in CRC incidence has been observed with intake of multivitamins, folate, calcium, statins, azathioprine, or 6-mercaptopurine. Nonsteroidal anti-inflammatory drugs and calcium have demonstrated benefits in patients with FAP and MAP, suggesting potential for reducing polyp incidence and recurrence. Colonoscopy and upper endoscopy should begin at ages 12 to 15 years in individuals with JPS, or earlier if symptoms are present. Surveillance should be repeated every 1 to 3 years, based on polyp burden. Polyps measuring at least 5 mm should be removed when feasible. The American Gastroenterological Association, as part of the United States Multisociety Task Force on Colorectal Cancer, recommends this approach to reduce CRC and gastric cancer risk, given the high lifetime risk of CRC (up to 39%) and the potential for dysplasia within juvenile polyps. Endoscopic polypectomy is first-line management for colorectal polyposis. Colectomy with ileorectal anastomosis is reserved for patients with CRC, endoscopically unmanageable polyp burden, or uncontrolled anemia from colonic bleeding. Proctocolectomy may be necessary for rectal cancer or advanced rectal polyposis. Surgical decisions should involve interprofessional expertise in hereditary polyposis syndromes.

Patients with colorectal polyps and polyposis syndromes are at increased risk for developing CRC. Early identification and treatment of these individuals are essential for reducing morbidity and mortality associated with CRC. Managing colorectal polyps and polyposis syndromes requires a collaborative, patient-centered approach to optimize outcomes. Healthcare professionals, including gastroenterologists, colorectal surgeons, pathologists, radiologists, geneticists, advanced practitioners, nurses, and pharmacists, involved in care must possess the clinical knowledge and skills necessary for diagnosis and clinical decision-making. Expertise includes recognition of clinical presentations, such as rectal bleeding, abdominal discomfort, and altered bowel habits, and initiation of appropriate evaluation pathways, including colonoscopy, CT colonography, and biopsy. Education of patients and caregivers regarding etiology, risk factors, and potential complications is an integral component of comprehensive care. A strategic approach is essential, incorporating evidence-based methods to optimize evaluation and treatment. Ethical considerations must guide clinical decision-making, ensuring informed consent and respect for patient autonomy in treatment choices. Each healthcare professional should understand their responsibilities and contribute specialized expertise to the patient’s care plan, supporting an interprofessional approach. Effective interprofessional communication enables seamless information exchange and collaborative decision-making among team members. Care coordination ensures that the patient’s journey from diagnosis through treatment and follow-up is well-managed, minimizing errors and enhancing safety. Adherence to principles of skill, strategy, ethics, defined responsibilities, interprofessional communication, and care coordination allows healthcare teams to provide patient-centered care, improve clinical outcomes, and enhance overall team performance in the management of colorectal polyps.