A salmon-colored lining, or mucosa, observed during an upper endoscopy is a significant finding requiring careful medical attention, though it rarely indicates immediate cancer. The inner lining of the esophagus is normally a pale pink color, and this change to a salmon shade is a visual sign of cellular change. This finding signals the presence of a condition that places an individual at a heightened risk for developing esophageal cancer over time.
What The Salmon Color Indicates
The salmon color is the hallmark visual indicator of a condition known as Barrett’s Esophagus (BE), a diagnosis made when the normal lining of the lower esophagus is replaced by a different type of tissue. The typical esophageal lining, called squamous epithelium, is flat and pale pink. In BE, it transforms into a columnar lining that is reddish or salmon-colored, a process called metaplasia.
This cellular change is an adaptive response to chronic irritation, most often caused by long-standing, severe gastroesophageal reflux disease (GERD). When stomach acid repeatedly flows back into the lower esophagus, the original squamous cells are damaged. The body attempts to protect itself by replacing them with a more acid-resistant tissue, similar to the lining of the intestine. This intestinal metaplasia, confirmed through a biopsy showing specialized cells, officially defines Barrett’s Esophagus.
The diagnosis is typically suspected when a physician sees the salmon-colored tissue extending at least one centimeter up into the esophagus from the junction with the stomach. However, the visual appearance alone is insufficient for a definitive diagnosis. Biopsy samples must be taken from the altered area and examined under a microscope to confirm the presence of intestinal metaplasia.
Understanding the Pathway to Cancer
Barrett’s Esophagus is classified as a pre-cancerous condition, meaning it is a precursor to esophageal adenocarcinoma. However, the progression is neither guaranteed nor common. The risk of developing cancer is low for most patients with BE, with the annual incidence of progression for non-dysplastic BE estimated to be less than 0.5% per year.
The progression to cancer follows a specific, multi-step pathway, which begins with the non-dysplastic BE tissue. The next step is the development of dysplasia, a term used to describe abnormal cell growth that is confined to the lining. Dysplasia is graded based on how abnormal the cells appear: low-grade dysplasia (LGD) or high-grade dysplasia (HGD).
LGD cells show minor architectural changes and represent a moderate risk of progression. HGD shows more severe abnormalities and is considered the last stage before the development of invasive esophageal adenocarcinoma. The risk of progression increases significantly as the grade of dysplasia rises.
For patients diagnosed with LGD, the annual risk of progression to HGD or cancer is approximately 1% to 2% per year. If HGD is present, the risk increases dramatically, with estimates ranging from 6% to 19% per year for progression to cancer. The presence and severity of dysplasia is the most important factor determining a patient’s risk profile and subsequent management plan.
Surveillance and Treatment Options
Once a diagnosis of Barrett’s Esophagus is confirmed, the primary management strategy focuses on two elements: controlling the underlying acid reflux and conducting regular surveillance. Aggressive management of acid reflux is achieved through lifestyle modifications and the long-term use of Proton Pump Inhibitors (PPIs), which are medications that significantly reduce stomach acid production.
For patients with non-dysplastic BE, surveillance involves routine follow-up endoscopies with systematic biopsies, typically performed every three to five years. This periodic monitoring is designed to detect the earliest signs of low-grade or high-grade dysplasia, which would signal the need for more aggressive intervention.
If high-grade dysplasia is detected, or if cancer is found at a very early stage, interventional procedures are often recommended to remove the abnormal tissue and prevent cancer progression. The preferred method for treating flat, dysplastic areas is Radiofrequency Ablation (RFA), which uses heat energy to destroy the superficial layer of abnormal mucosa.
For any visible, raised areas or nodules within the BE segment, Endoscopic Mucosal Resection (EMR) is performed first to remove the tissue for detailed pathology analysis. Both RFA and EMR are highly effective treatments that can eliminate the dysplastic tissue without requiring major surgery. These endoscopic eradication therapies are successful in over 90% of cases for eliminating dysplasia.