A Sessile Serrated Adenoma (SSA), also known as a Sessile Serrated Polyp (SSA/P), is a specific type of colorectal polyp with a unique risk profile for developing into colorectal cancer. These lesions are recognized as a distinct precursor to cancer, separate from conventional adenomas. While most colorectal cancers follow the traditional adenoma-carcinoma sequence, SSA/Ps are responsible for up to 30% of all colorectal cancers. Their subtle appearance and unique progression mechanism challenge detection and complete removal, directly impacting long-term cancer risk.
Defining the Sessile Serrated Adenoma
A Sessile Serrated Adenoma is characterized by its subtle, flat shape, meaning it does not protrude significantly into the colon’s interior like a mushroom-shaped polyp. This flat morphology, often combined with indistinct borders and a pale color, makes the SSA/P difficult for a colonoscopist to identify. SSA/Ps are most frequently discovered in the right side of the colon, where the quality of the bowel preparation can sometimes be less optimal, further complicating detection.
The internal structure of an SSA/P distinguishes it histologically from other polyps, exhibiting a characteristic serrated pattern of the crypts, the small glands lining the colon. A microscopic feature is the dilation and lateral spreading of these crypts at the base of the lesion, often creating an L or boot shape. Unlike conventional adenomas, SSA/Ps typically lack classic nuclear atypia at first, but their architectural distortion confirms their neoplastic nature. This difference often leads to a higher rate of incomplete removal compared to conventional adenomas.
The Serrated Neoplasia Pathway
The cancer risk associated with SSA/Ps stems from their progression through a unique molecular route called the serrated neoplasia pathway. This pathway is defined by specific genetic and epigenetic changes that can lead to rapid tumor growth. The initial and most pronounced molecular event in most SSA/Ps is an activating point mutation in the BRAF oncogene.
The BRAF mutation is linked to the CpG island methylator phenotype (CIMP), where widespread methyl groups are added to gene promoter regions. This hypermethylation can silence tumor-suppressor genes that regulate cell growth and repair. In a subset of SSA/Ps, this process leads to the silencing of the DNA mismatch repair gene \(MLH1\). The loss of \(MLH1\) function results in high microsatellite instability (MSI-H), accelerating the accumulation of mutations and speeding progression to invasive cancer. This potential for rapid transformation explains why SSA/Ps are strongly implicated in the development of “interval cancers,” found between recommended surveillance colonoscopies.
Identification and Polypectomy
Detecting a Sessile Serrated Adenoma presents a significant challenge due to its flat appearance and tendency to be covered by mucus, making it easy to overlook during a standard colonoscopy. Endoscopists employ specialized techniques to improve visualization, such as high-definition scopes or chromoendoscopy, which involves applying a dye to highlight subtle mucosal changes. Narrow band imaging (NBI) is another tool that uses specific light filters to enhance the visibility of the lesion’s vascular pattern and surface structure.
Once identified, the standard treatment for an SSA/P is complete endoscopic removal, known as polypectomy. Because these polyps have indistinct borders and a high rate of incomplete removal, the resection technique is important. Smaller lesions, typically less than 10 millimeters, are often removed using cold snare polypectomy. Larger SSA/Ps, especially those between 10 and 20 millimeters, frequently require endoscopic mucosal resection (EMR). EMR involves injecting a solution beneath the lesion to lift it away from the colon wall, allowing for more complete removal. The goal is to achieve clear margins by taking a rim of normal tissue, as incomplete removal increases the risk of recurrence and subsequent cancer development.
Personalized Surveillance Recommendations
Following the removal of an SSA/P, the focus shifts to personalized surveillance to manage the patient’s long-term risk. The interval for the next colonoscopy is determined by risk stratification factors, including the size and number of the removed polyps, and whether the lesion showed signs of dysplasia. Current guidelines from major medical societies provide a clear framework for managing this risk.
Surveillance intervals are determined by the burden of disease. These recommendations assume a high-quality initial procedure with complete removal and adequate bowel preparation. If a large SSA/P was removed in pieces, an early repeat colonoscopy, often within six months, is necessary to verify the resection site is clear of residual tissue.
The surveillance intervals are typically structured as follows:
- Patients with one or two SSA/Ps less than 10 millimeters without dysplasia are recommended a follow-up in five to ten years.
- Patients with three to four small SSA/Ps typically mandate a follow-up in three to five years.
- A three-year surveillance interval is recommended for patients with any SSA/P 10 millimeters or larger.
- A three-year surveillance interval is also recommended for those with five to ten SSA/Ps, or any SSA/P that showed signs of high-grade dysplasia.
Adherence to this personalized surveillance schedule is important for managing the risk posed by the serrated pathway, allowing for the early detection and removal of new or recurrent lesions.