Colon polyps

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Colon polyps are unregulated growth of mucosal surface of the colon. The exact etiology is unclear. However, risk factors may contribute to the formation of polyps including age,family history, obesity, cigarette smoking, and alcohol consumption. There are four different types of polyps including inflammatory, hamartomatous, serrated, and adenomatous polyps, which have different pathogenesis. Inflammatory polyps are non-neoplastic polyps that occur following intestinal inflammation, infections, or ischemia. Hamartomatous polyp is an overgrowth of mature cells and connective tissue elements including smooth muscle, lamina propria, and cartilage, and fat which is covered by a hypertrophic epithelium. Serrated polyps include hyperplastic, sessile serrated and traditional serrated polyps. Hyperplastic polyps are the most common polyps. Hyperplastic polyp is infolding of the cryptepithelium that forms serration or saw-toothed appearance. Sessile serrated polyps are flask-shaped crypts, with dilatation and branching but not pedunculated. Traditional serrated adenomas are serrated polyps that are protuberant and pedunculated, which are located in left colon. Traditional adenoma also known as conventional polyps, are developed throughout the colon. They are the most prevalent polyps that have malignant potential. Colon polyps are incidentally found in colonoscopies and sigmoidoscopies. Polyps might grow gradually and cause symptoms including obstruction, bleeding, and changes in bowel habits. Some of them might progress to colorectal cancer. Colonoscopy and flexible sigmoidoscopy are diagnostic studies of choice to diagnose colon polyps. The mainstay of treatment for colon polyps is surgery. Aspirin is recommended to prevent recurrent polyps or conversion of colon polyps to colorectal cancer. Surgery is indicated for all colon polyps that are detected during screening for colorectal cancer. There are different surgical treatments for colon polyps including polypectomy, laparoscopic surgery and total proctocolectomy. All polyps must be sent to pathology laboratory for the biopsy. Regular exercise, healthy diet, smoking cessation, and reduced alcohol consumption might be helpful for preventing colon polyps. It is recommended to take aspirin, calcium and vitamin D to decrease the risk of colon polyps. According to guidelines for colonoscopysurveillance after screening and polypectomy by the US Multi-Society Task Force on colorectal cancer, surveillance and screening are more frequent after first or second adenomatous polyps or serrated polyps.

In 1895, the first sigmoidoscopy was developed to visualize the colon. Since then, it has been used to screen for colon polyps and colorectal cancer. In 1975, it was reported that adenomas are the precursors of colorectal cancer and hyperplastic polyps are non-neoplastic lesions. Since 1992, different pathways of polyp-cancer have been introduced, including molecular adenoma-carcinoma progression, mutator phenotype, serrated (neoplasia) pathway.

Colon polyps may be classified into two groups of neoplastic and nonneoplastic. Non-neoplastic polyps consist of inflammatory and hamartomatous polyps. Neoplastic polyps consist of serrated and adenomatous polyps. Adenomatous polyps may be classified into several subtypes based on endoscopic, histologic features and degree of dysplasia. Adenomas may be classified according to endoscopic features into four groups including sessile, pedunculated, flat, or depressed. Adenomas may be classified according to histologic features into three groups including tubular, tubulovillous, and villous.

Any form of unregulated growth in the colon may cause polyps. The exact etiology is unclear. However, risk factors may contribute to the formation of polyps. There are four different types of polyps including inflammatory, hamartomatous, serrated, and adenomatous polyps, which have different pathogenesis. Inflammatory polyps are non-neoplastic polyps that occur following intestinal inflammation, infections, or ischemia. Hamartomatous polyp is an overgrowth of mature cells and connective tissue elements including smooth muscle, lamina propria, and cartilage, and fat. They are covered by a hypertrophic epithelium. Serrated polyps are different polyps which have variable malignant potential. They include hyperplastic, sessile serrated and traditional serrated polyps. Hyperplastic polyps are the most common polyps. Hyperplastic polyp is infolding of the cryptepithelium that forms serration or saw-toothed appearance. Sessile serrated polyps are flask-shaped crypts, with dilatation and branching but not pedunculated. Traditional serrated adenomas are serrated polyps that are protuberant and pedunculated, which are located in left colon. Traditional adenoma also known as conventional polyps, are developed throughout the colon. They are the most prevalent polyps that have malignant potential.

The cause of colon polyps has not been identified.

Colon polyps might present solitary or multiple. Solitary colon polyps usually have no symptoms. Colon polyps must be differentiated from other genetic diseases that cause multiple polyps, such as Peutz–Jeghers syndrome, Cowden syndrome, Bannayan–Riley–Ruvalcaba syndrome, juvenile polyposis, and McCune–Albright syndrome.

The exact incidence and prevalence of colon polyps are unknown. Colon polyps are incidentally found in colonoscopies and sigmoidoscopies. However, the incidence of colon polyps is estimated to be 200,000 cases in the united states annually. The prevalence of colon polyps is between 10-25% in different screening studies. The incidence of colon polyps increases with age; the median age at diagnosis is 50 years. Colon polyps usually affect individuals of the African American race. Men are more commonly affected by colon polyps than women. Colon polyps is a common disease worldwide.

Risk factors in the development of colon polyps may be environmental, genetic, and lifestyle behaviors. The most potent risk factor in the development of colon polyps is age. Other risk factors include family history, obesity, cigarette smoking, and alcohol consumption.

There is insufficient evidence to recommend routine screening for colon polyps. According to the guidelines screening for the colon polyps must be done earlier after the first colon polyps are discovered. Hyperplastic polyps have no malignant tendency and recommendation for the colonoscopy is similar to general population. Adenomatous and serrated polyps have neoplastic nature and must be followed every 3-5 years.

Colon polyps are very common in general population. They are usually found during screening colonoscopy. Polyps might grow gradually and cause symptoms including obstruction, bleeding, and changes in bowel habits. Some of them might progress to colorectal cancer. Therefore, it is advisable to resect all polyps that are found during colonoscopy and send the tissue biopsy for pathology. Prognosis of colon polyps is generally excellent. The presence of multiple polyps is associated with genetic disorders with a particularly poor prognosis.

Colonoscopy and flexible sigmoidoscopy are diagnostic studies of choice to diagnose colon polyps.

The majority of patients with colon polyps are asymptomatic. Patients with colon polyps may have a positive history of previous polyps. Family history of polyps might be positive. Colon polyps are incidentally found during screening for colon cancer. However, if the polyps are large, they might present with rectal bleeding and fatigue, change in bowel habits and stool color, and crampy abdominal pain.

Patients with colon polyps usually have normal physical examination. Patients with large colon polyps might have few signs including abdominal tenderness in the lower abdomen, a palpable rectal mass on digital rectal exam, and pallor due to occult bleeding.

Laboratory testing is usually normal among patients with colon polyps. However, some patients with colon polyps may have abnormal tests, including CBC and stool test, which is usually suggestive of gastrointestinal bleeding. They might present with anemia or positive fecal occult blood.

There are no ECG findings associated with colon polyps.

Double-contrast Barium enema may be helpful in the diagnosis of colon polyps. Colon polyps might be presented as an outgrowths with lobulation or indentation and filling defects on x-rays.

There are no echocardiography/ultrasound findings associated with colon polyps.

CT scan with contrast and CT colonography or virtual colonoscopy may be helpful in the diagnosis of colon polyps. Outgrowths and filling defects are suggestive of colon polyps.

MRI may be helpful in the diagnosis of colon polyps. Diffusion-weighted magnetic resonance imaging (DWI) and MRI colonography are used to detect polyps.

Colonoscopic spectroscopy and narrow-band imaging (NBI) may be helpful in the diagnosis of colon polyps.

Colonoscopy is considered as a gold standard for evaluating intestine, diagnostic and therapeutic approaches. Tissue biopsy and polypectomy could be done during colonoscopy. Findings on a colonoscopy and flexible sigmoidoscopy suggestive of colon polyps include visual detection of an outgrowth. Colonoscopy has 0.02% mortality and 0.2% morbidity 0.2%. Colonoscopy has side effects including pain, risk of perforation and bleeding.

The mainstay of treatment for colon polyps is surgery. Aspirin is recommended to prevent recurrent polyps or conversion of colon polyps to colorectal cancer.

Surgery is the mainstay of treatment for colon polyps. Surgery is indicated for all colon polyps that are detected during screening for colorectal cancer. There are different surgical treatments for colon polyps including polypectomy, laparoscopic surgery and total proctocolectomy. All polyps must be sent to pathology laboratory for the biopsy.

Effective measures for the primary prevention of colon polyps include lifestyle changes, medications, and genetic counseling. Regular exercise, healthy diet, smoking cessation, and reduced alcohol consumption might be helpful for preventing colon polyps. It is recommended to take aspirin, calcium and vitamin D to decrease the risk of colon polyps.

Effective measures for the secondary prevention of colon polyps include surveillance after finding polyps on routine screening. According to guidelines for colonoscopysurveillance after screening and polypectomy by the US Multi-Society Task Force on colorectal cancer, surveillance and screening are more frequent after first or second adenomatous polyps or serrated polyps. Hyperplastic polyps are considered benign and screening remains similar to general population.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

In 1895, the first sigmoidoscopy was developed to visualize the colon. Since then, it has been used to screen for colon polyps and colorectal cancer. In 1975, it was reported that adenomas are the precursors of colorectal cancer and hyperplastic polyps are non-neoplastic lesions. Since 1992, different pathways of polyp-cancer have been introduced, including molecular adenoma-carcinoma progression, mutator phenotype, serrated (neoplasia) pathway.

• In 1895, the first rigid sigmoidoscope was developed at Hopkins by Kelly.^[1]
• In 1927, Lockhart-Mummery and Dukes recognized the precancerous changes in the rectum and colon and identified the staging system for colorectal cancer.^[2]
• In 1960, Hertz and Deddish reported using sigmoidoscopy to screen colorectal cancer with 90% survival rate followed for over 15 years.^[1]
• In 1967, Greegor used guaiac card test to detect early-stage colorectal cancer.^[3]
• In 1973, Wolff and Shinya used colonoscopy to remove polyps.^[4]
• In 1975, Morson was the first who reported that adenomas are the precursors of colorectal cancer and hyperplastic polyps are non-neoplastic lesions.^[5]
• In 1988, Vogelstein introduced molecular adenoma-carcinoma progression model which APC mutations are the initiator factors, known as a classic adenoma-carcinoma pathway.^[6]
• In 1992, another pathway known as the mutator phenotype was discovered in HNPCC patients.^[7]
• In 1993, the polyp-cancer sequence was accepted by the National Polyp Study.^[8]
• In 1999, Jass demonstrated another pathway related to serrated polyps, known as “serrated (neoplasia) pathway.”^[7]

• In 1973, Wolff and Shinya used colonoscopy to remove polyps.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Colon polyps may be classified into two groups of neoplastic and non-neoplastic. Non-neoplastic polyps consist of inflammatory and hamartomatous polyps. Neoplastic polyps consist of serrated and adenomatous polyps. Adenomatous polyps may be classified into several subtypes based on endoscopic and histologic features, and degree of dysplasia. Adenomas may be classified according to endoscopic features into four groups including sessile, pedunculated, flat, or depressed. Adenomas may be classified according to histologic features into three groups including tubular, tubulovillous, and villous.

• Colon polyps may be classified into several subtypes based on:^{[1][2][3][4][5]}
  • Malignancy potentials
  • Endoscopic features
  • Histologic features
  • Degree of dysplasia

Colon polyps may be classified according to the NBI International Colorectal Endoscopic (NICE) classification into two types:^[6][7]

NICE criterion	Type 1	Type 2
Color	Same or lighter background	Darker background
Vessels	None, or isolated lacy vessels coursing across the lesion	Brown vessels surrounding the white center
Surface	Circular pattern with dark or white small spots surrounded by lighter mucosa	Oval, tubular, or branched white structures
Probable pathology	Hyperplastic	Adenoma

Colon polyps may be classified according to malignancy potentials into two large groups:

• Non-neoplastic
  • Inflammatory polyps
    • Inflammatory pseudopolyps
    • Prolapse type inflammatory polyps
    • Myoglandular polyps
  • Hamartomatous polyps
    • Juvenile polyps
    • Peutz-Jeghers syndrome
    • Cronkhite-Canada syndrome
    • Phosphatase and tensin homolog (PTEN) hamartoma tumor syndrome
• Neoplastic
  • Serrated polyps
    • Hyperplastic polyps
    • Traditional serrated adenomas
    • Sessile serrated polyps
    • Serrated polyposis syndrome
  • Adenomatous polyps

Adenomas may be classified according to endoscopic features into four groups:

• Sessile
• Pedunculated
• Flat
• Depressed

Adenomas may be classified according to histologic features into three groups:

• Tubular
• Villous
• Tubulovillous

Adenomas may be classified according to degree of dysplasia into two groups:

• Low-grade dysplasia
• High-grade dysplasia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Any form of unregulated growth in the colon may cause polyps. The exact etiology is unclear. However, risk factors may contribute to the formation of polyps. There are four different types of polyps including inflammatory, hamartomatous, serrated, and adenomatous polyps, which have different pathogenesis. Inflammatory polyps are non-neoplastic polyps that occur following intestinal inflammation, infections, or ischemia. Hamartomatous polyp is an overgrowth of mature cells and connective tissue elements including smooth muscle, lamina propria, and cartilage, and fat. They are covered by a hypertrophic epithelium. Serrated polyps are different polyps which have variable malignant potential. They include hyperplastic, sessile serrated and traditional serrated polyps. Hyperplastic polyps are the most common polyps. Hyperplastic polyp is infolding of the crypt epithelium that forms serration or saw-toothed appearance. Sessile serrated polyps are flask-shaped crypts, with dilatation and branching but not pedunculated. Traditional serrated adenomas are serrated polyps that are protuberant and pedunculated, which are located in left colon. Traditional adenoma also known as conventional polyps, are developed throughout the colon. They are the most prevalent polyps that have malignant potential.

• Any form of unregulated growth in the colon may cause polyps. The exact etiology is unclear. However, risk factors may contribute to the formation of polyps.^[1][2][3][4]
• There are four different types of polyps including inflammatory, hamartomatous, serrated, and adenomatous polyps, which have different pathogenesis.
• The pathophysiology of colon polyps depends on the histological type.

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• Inflammatory polyps are non-neoplastic polyps that occur following intestinal inflammation, infections, or ischemia.^[2][5]
• They mostly occur in patients with inflammatory bowel disease, mainly ulcerative colitis.
• They are considered as pseudopolyps which contain inflammatory infiltrations with distorted mucosa.
• It had no malignant potential. However, it is recommended to biopsy the lesion and surrounding mucosa.
• Microscopic pathology of biopsy shows mixture of normal, ulcerated, and regenerating mucosa which is surrounded by areas of mucosal loss.

• Hamartomatous polyp is an overgrowth of mature cells and connective tissue elements including smooth muscle, lamina propria, and cartilage, and fat. They are covered by a hypertrophic epithelium.^[6]
• They might be pedunculated, inflamed, or smooth polyps which are solitary or multiple.
• Solitary hamartomatous polyps, also known as juvenile polyps, can present more commonly in younger population.
• Solitary polyps has no significant risk of cancer. However, multiple polyps of the colon have a 10% risk of malignancy.

• Serrated polyps are different polyps which have variable malignant potential. They include hyperplastic, sessile serrated and traditional serrated polyps. They have various histopathologies and manifestations:
  • Hyperplastic polyps are the most common polyps.
    • They are small outpouching, less than 5 mm, which are located mostly in rectosigmoid area.
    • Hyperplastic polyp is infolding of the crypt epithelium that forms serration or saw-toothed appearance.
    • The molecular basis of this transformation is still unclear. However, it has been attributed to failure of apoptosis.
    • BRAF mutations are associated with crypt serration.^[7]
    • There are three different subtypes of hyperplastic polyps based on degree of serration and content, including microvesicular type, goblet cell–rich type, and mucin-poor type.
  • Sessile serrated polyps:
    • They are flask-shaped crypts, with dilatation and branching but not pedunculated.^[8][9]
    • Crypts grow along muscularis mucosae and creating inverted T- or L-shaped appearance.
    • Serration happens at the base and bottom of the crypts.
  • Traditional serrated adenomas:
    • They are protuberant and pedunculated polyps, less than 1.5 cm, which are located in left colon.^[5]
    • They have cytological dysplasia including nuclear transformation, irregular nuclear polarity, and serration.
    • Cytological dysplasia causes crypts that are irregular and branching.

• Traditional adenoma also known as conventional polyps, are developed throughout the colon.
• They are the most prevalent polyps that have malignant potential.
• They have different gross appearances including pedunculated, sessile, flat, or depressed.
• They might have different histopathologies including tubular, villous, or tubulovillous.

• The development of colon polyps is the result of multiple genetic mutations.
• Genetic mutations might cause hereditary polyps disorders.

• FAP is due to mutations in the following genes:
  • APC gene, which is located on chromosome 5 in band q21 or band q22 (5q21-q22).
  • MUTYH gene, which is located on chromosome 1 between bands p34.2 and p32.1 (5p34.3-p32.1).
  • MYH-associated polyposis (MAP) is caused by mutations in the MYH gene.

Peutz-Jeghers syndrome

• It is thought that Peutz-Jeghers syndrome is the result of deletion or partial deletion of STK11 (LBK1) gene, located on chromosome 19p13.3.

Gardner’s syndrome

• It is caused by mutation in the APC gene located in chromosome 5q21 (band q21 on chromosome 5). 

Serrated polyposis syndrome

• They develop multiple serrated adenomatous polyps in the upper part of the colon.

• It is an autosomal dominant disorder. 
• It increases risk of colorectal cancer.
• It has extra-colonic tumors. 
• There has been some association with the following genes:
  • SMAD4 on chromosome 18.
  • PTEN on chromosome 10.

• On gross pathology, outpouching, pedunculated or flat lesions are characteristic findings of colon polyps.
• On gross pathology, colon polyps may have a short or long stalk.
• The polyp might have hemorrhagic stalk and colon wall with pale ribbon of mucosal covering.

• On microscopic histopathological analysis, serration of the luminal surface and normal nuclei are characteristic findings of hyperplastic polyps.
• On microscopic histopathological analysis, branched tubular glands are characteristic findings of tubular adenoma.
• On microscopic histopathological analysis, long finger-like projections are characteristic findings of villous adenoma.
• On microscopic histopathological analysis, branched and dilated glands, no cytological atypia, eosinophilic cytoplasm, and luminal epithelial tufting are characteristic findings of sessile serrated adenoma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The cause of colon polyps has not been identified. To review risk factors for the development of colon polyps, click here.

• The exact etiology of colon polyps is unknown.^[1][2]
• There are many genetic and environmental risk factors which increase the risk of development of colon polyps.
• To review risk factors for the development of colon polyps, click here.

​​​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Colon polyps might present solitary or multiple. Solitary colon polyps usually have no symptoms. Colon polyps must be differentiated from other genetic diseases that cause multiple polyps, such as Peutz–Jeghers syndrome, Cowden syndrome, Bannayan–Riley–Ruvalcaba syndrome, juvenile polyposis, and McCune–Albright syndrome.

Colon polyps must be differentiated from the following diseases:^[1][2]

• Peutz–Jeghers syndrome
• Cowden syndrome
• Cronkhite–Canada syndrome
• Bannayan–Riley–Ruvalcaba syndrome
• Juvenile polyposis
• McCune–Albright syndrome

Differential diagnosis according to polys:

Diseases	History and Symptoms				Physical Examination			Laboratory Findings				Other Findings
	Abdominal Pain	Rectal Bleeding	Hyperpigmentation	Fatigue	Abdominal Tenderness	Hyperpigmentation	Anemia	Gene(s)	Sertoli Cell Tumors	Gastrointestinal Tumors	Cancers
Juvenile Polyposis Syndrome	+	_	–	+	–	–	–	SMAD4 BMPR1A	–	Adenoma+  Hamartoma+++	Colon	_
Cowden Syndrome	–	–	Axillary+ Inguinal+ Facial+	–	–	Axillary+ Inguinal+ Facial+	–	PTEN	–	Adenoma+  Hamartoma+++	Breast Thyroid Endometrium	Trichilemmoma skin hamartoma Hyperplastic polyps macrocephaly breast fibrosis
Carney Syndrome	–	–	Facial+ Mucosal+	–	–	Facial+ Mucosal+	–	PRKAR1A	++		Thyroid	Myxomas of skin and heart
Familial Adenomatous Polyposis	+	+	–	+	+/–	–	+	APC	–	Adenoma+++	Colon brain	Desmoid tumors Osteomas
Hereditary Non–Polyposis Colon Cancer	–	+	–	+	+/–	–	+	MLH1 MSH2 MSH3 MSH6 PMS1 PMS2	–	Adenoma+	Endometrial Gastric renal pelvis ureter Ovarian	Sebaceous adenoma

Differential of gastrointestinal bleeding

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo– tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Colon polyps + – – – – – – – + – – – – Colonoscopy Peutz–Jeghers syndrome Depends on location of polyps it maybe present ± – ± – ± ± ± Rectal bleeding may be present due to polyp – – – + Hamartomatous polyps present on endoscopy Iron deficiency anemia on CBC STK11 mutation Intra–operative enteroscopy (laparatomy with endoscopy Double balloon eneteroscopy Colonoscopy Barium Swallow Can lead to colon cancer, breast cancer, ovarian cancer, cervical cancer, and testicular cancer Peptic ulcer disease Diffuse ± − + − − − + Gastric ulcer– melena and hematemesis Duodenal ulcer– melena and hematochezia Positive if perforated Positive if perforated Positive if perforated N Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis Gastritis Epigastric ± − + − − − Positive in chronic gastritis + − − − N H.pylori infection diagnostic tests Endoscopy H.pylori gastritis guideline recommendation Gastrointestinal perforation Diffuse + ± – ± − − − + + + ± Hyperactive/hypoactive WBC> 10,000 Air under diaphragm in upright CXR Hamman’s sign Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti–neutrophil cytoplasmic antibody (P–ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn’s disease String sign on abdominal x–ray in Crohn’s disease Extra intestinal findings: Uveitis Arthritis Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR CT scan Bowel wall thickening Edema Colon carcinoma Diffuse/localized − − − − ± ± + + ± − − Normal or hyperactive if obstruction present CBC Carcinoembryonic antigen (CEA) Colonoscopy Flexible sigmoidoscopy Barium enema CT colonography  PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction Budd–Chiari syndrome RUQ ± − − ± − − − Positive in liver failure leading to varices − − − N Elevated serum aspartate aminotransferase and alanine aminotransferase levels may be more than five times the upper limit of the normal range. Elevated serum alkaline phosphatase and bilirubin levels, decreased serum albumin level. Findings on CT scan suggestive of Budd–Chiari syndrome include: Early enhancement of the caudate lobe and central liver around the inferior vena cava Delayed enhancement of the peripheral liver with accompanying central low density (flip–flop appearance) Peripheral zones of the liver show reversed portal venous blood flow In the chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas Ascitic fluid examination shows: Total protein more than 2.5 g per deciliter White blood cells are usually less than 500/μL. Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N >60% TS >240 μg/L SF Raised LFT Hyperglycemia Ultrasound shows evidence of cirrhosis Extra intestinal findings: Hyperpigmentation Diabetes mellitus Arthralgia Impotence in males Cardiomyopathy Atherosclerosis Hypopituitarism Hypothyroidism Extrahepatic cancer Prone to specific infections Cirrhosis RUQ − − − + − − + + + − − N Hypoalbuminemia Prolonged PT Abnormal LFTs Hyponatremia Thrombocytopenia US Nodular, shrunken liver Ascites Stigmata of liver disease Cruveilhier– Baumgarten murmur Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent Leukocytosis and lactic acidosis Amylase levels D–dimer CT angiography SMA or SMV thrombosis Also known as abdominal angina that worsens with eating Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Leukocytosis Abdominal x–ray Distension and pneumatosis CT scan Double halo appearance, thumbprinting Thickening of bowel May lead to shock Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N Fibrinogen D–dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra–abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The exact incidence and prevalence of colon polyps are unknown. Colon polyps are incidentally found in colonoscopies and sigmoidoscopies. However, the incidence of colon polyps is estimated to be 200,000 cases in the united states annually. The prevalence of colon polyps is between 10,000-25,000 in 100,000 screening studies. The incidence of colon polyps increases with age; the median age at diagnosis is 50 years. Colon polyps usually affect individuals of the African American race. Men are more commonly affected by colon polyps than women. Colon polyps is a common disease worldwide.

• The incidence of colon polyps is estimated to be 200,000 cases in the united states annually.
• The cumulative incidence of polyps in 3 years after normal flexible sigmoidoscopy is 7%.^[1]
• The cumulative incidence of polyps in 3 years after normal colonoscopy is 27%.^[1]

• The prevalence of colon polyps is 10,000 in 100,000 sigmoidoscopy studies.^[1]
• The prevalence of colon polyps is 25,000 in 100,000 colonoscopy studies.^[1]
• The prevalence of hyperplastic colon polyps in autopsy studies is between 7,000-40,000 in 100,000 in individuals younger than 50 years of age.^[2]
• The prevalence of hyperplastic colon polyps in autopsy studies is between 20,000-40,000 in individuals older than 50 years of age.^[2]

• The incidence of colon polyps increases with age; the median age at diagnosis is 50 years.
• Colon polyps commonly affects individuals older than 50 years of age.

• Colon polyps usually affect individuals of the African American race.^[3]

• Men are more commonly affected by colon polyps than women.^[3]

• Colon polyps is a common disease worldwide.

​​ ​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Risk factors in the development of colon polyps may be environmental, genetic, and lifestyle behaviors. The most potent risk factor in the development of colon polyps is age. Other risk factors include family history, obesity, cigarette smoking, and alcohol consumption.

• Risk factors in the development of colon polyps may be modifiable or nonmodifiable factors.^[1][2][3][4]
• Risk factors in the development of colon polyps may be environmental, genetic, and lifestyle behaviors.
• The most potent risk factor in the development of colon polyps is age.
• Other risk factors include family history, obesity, cigarette smoking, and alcohol consumption.

• Common risk factors in the development of colon polyps include:
  • Non-modifiable
    • Age
    • Race
    • Past history of colon polyps
    • Family history
    • Inflammatory bowel disease
  • Modifiable lifestyle behavior
    • Cigarette smoking
    • Alcohol abuse
    • Obesity
    • Lack of exercise
    • Diet high in red meats and processed meats
    • Low fiber intake
    • Low calcium intake
    • Low folate intake
    • Type 2 diabetes mellitus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

There is insufficient evidence to recommend routine screening for colon polyps. According to the guidelines screening for the colon polyps must be done earlier after the first colon polyps are discovered. Hyperplastic polyps have no malignant tendency and recommendation for the colonoscopy is similar to general population. Adenomatous and serrated polyps have neoplastic nature and must be followed every 3-5 years.

• There is insufficient evidence to recommend routine screening for colon polyps in general population.
• According to guidelines for colonoscopy surveillance after screening and polypectomy by the US Multi-Society Task Force on Colorectal Cancer, recommendations for surveillance and screening are as follows:^[1][2][3]

Baseline colonoscopy			Recommendation
No polyps			Colonoscopy every 10 years
Polyps	Hyperplastic polyps	Size <10 mm	Colonoscopy every 10 years
	Adenomatous polyps	1-2 tubular adenomas <10 mm	Colonoscopy every 5-10 years
		3-10 tubular adenomas <10 mm	Colonoscopy every 3 years
		>10 adenomas	Colonoscopy <3 years
		Tubular adenomas ≥10 mm	Colonoscopy every 3 years
		Villous adenomas	Colonoscopy every 3 years
		Adenoma with high grade dysplasia	Colonoscopy every 3 years
		No adenoma after first low-risk adenoma	Colonoscopy every 10 years
		No adenoma after first high-risk adenoma	Colonoscopy every 5 years
	Second adenomatous polyps	Second low-risk adenoma	Colonoscopy after 5 years
		High-risk adenoma following low-risk adenoma	Colonoscopy every 3 years
		Low-risk adenoma following high-risk adenoma	Colonoscopy after 5 years
		Second high-risk adenoma	Colonoscopy every 3 years
	Serrated polyps	Sessile serrated polyp(s) <10 mm with no dysplasia	Colonoscopy every 5 years
		Sessile serrated polyp(s) ≥10 mm	Colonoscopy every 3 years
		Sessile serrated polyp with dysplasia	Colonoscopy every 3 years
		Traditional serrated adenoma	Colonoscopy every 3 years
		Serrated polyposis syndrome	Colonoscopy every year

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Colon polyps are very common in general population. They are usually found during screening colonoscopy. Polyps might grow gradually and cause symptoms including obstruction, bleeding, and changes in bowel habits. Some of them might progress to colorectal cancer. Therefore, it is advisable to resect all polyps that are found during colonoscopy and send the tissue biopsy for pathology. Prognosis of colon polyps is generally excellent. The presence of multiple polyps is associated with genetic disorders with a particularly poor prognosis.

• Colon polyps are very common in general population.^[1]
• They are usually found during screening colonoscopy.^[2]
• Polyps might grow gradually and cause symptoms including obstruction, bleeding, and changes in bowel habits.
• Some of them might have malignant potential.
• If left untreated, it may progress to develop colorectal cancer. The progression from an adenomatous polyp to colorectal cancer may take 10-15 years. 
• All polyps are recommended to be resected.

• Common complications of colon polyps include:^[2][3]
  • Colorectal cancer

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• Gastrointestinal bleeding
• Bleeding following polypectomy

• Prognosis of colon polyps is generally excellent.^[1]
• The presence of multiple polyps is associated with genetic disorders with a particularly poor prognosis.
• Colon polyps that are associated with BRAF and KRAS mutations have a poor prognosis.^[4] This study also found no increase in mortality if 3 or more adenomas (RR = 1.4 [95% CI, 0.6 to 3.0]) or polyps larger than 1 cm

Risk of cancer over time after initial polypectomy in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer randomized clinical trial^[5] In addition, the study found no difference in cancer risk among “participants with 3 or more nonadvanced adenomas and those with no adenomas (RR, 1.4 [95% CI, 0.6 to 3.0]” and no difference based on polyp size great than 1 cm.

	Cancer cases after 13 years % (n)	Cancer incidence rates (per 10 000 person-years of observation)	Cancer mortality compared to persons with no adenoma (relative risk)
No adenoma n = 94,248	< 0.1% (71)	7.1	NA
Nonadvanced adenoma n = 65,650	< 0.1% (55)	9.1	1.2 (95% CI, 0.5-2.7)
Advanced adenoma n = 34,993 (≥1 cm, high-grade dysplasia, or tubulovillous or villous histology)	0.2% (70)	20	2.6 (95% CI, 1.2-5.7)

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