Hello! Welcome to the Thoracic Oncology course. My name is Aarti Bedi, I'm one of the advanced endoscopist here at the University of Michigan and the Department of Gastroenterology. Today we're going to be talking about endoscopic TN staging and management of early stages of esophageal cancer. This is a big topic, this is what I do everyday and I love, so it was a little difficult for me to be able to scram all this stuff in for you guys. We actually divided this into a few parts. So we're going to have part one, two, and three and I will see you for all of those. The objectives for part one are going to be reviewing the esophageal wall anatomy which is critical for everything that we're going to talk about and you're going to come to see that very shortly. And we're going to review briefly esophageal cancer so you know what it is we're talking about and what we're dealing with before we discuss how to manage it and how to stage it. One of our pre-lecture questions that I'm going to introduce to you is as follows. I'd like for you guys to keep these questions in mind whenever we're going through the lecture itself to see if you can pick up on what the answer is and the justification and the reasoning behind it. So the first question is, let's figure out what is the correct esophageal wall anatomy going from the luminal to the mediastinal surface. A is lamina propria, muscularis propria, submucosa, muscularis mucosa and then adventitia. B is lamina propria, submucosa, muscularis mucosa, adventitia and serosa. C, lamina propria, muscularis mucosa, submucosa, muscularis propria and adventitia. D, lamina propria, muscularis mucosa, submucosa, adventitia and serosa. A lot of words there. But hopefully by the end of this structure you guys would be able to figure that out. Question number two, is looking at the risk factor for esophageal adenocarcinoma. So all of the following are risk factor for esophageal adenocarcinoma except A, alcohol B, gastroesophageal reflux disease or GERD, C, obesity, D, tobacco, E, Barret's Esophagus. Question number three, the most optimum assessment of treatment effect post radiation therapy and chemotherapy is, A, EUS. B, CT, C, MRI, or D, FDG-PET imaging. Number four, tumor extending into the submucosa would be staged as what? T1a, T1b, T2, T3, or T4? Number five, the most accurate way to obtain information on pre-treatment T staging is A, EGD with FNA, FNA stands for fine needle aspiration. B, EUS, C, a PET-CT, D, a regular CT, or E, MRI. Let's start out by getting an overview of esophageal cancer. This is some sears data and this shows that the incident of esophageal cancer if you look, represents about 1% of all the new cancer cases in the United States. It ranks about 18th in the most common types of cancer with number one and number two being breast and lung, as you can see here. An interesting thing to note though, as time has progressed and if medical therapy is involved and progressed as well, we're seeing that these patients are surviving. As you can see in 1975, the five year related survival was only 4%, which is really dismal. And if you look at in 2007, there's up to 21.6%. And I think that's in part, not only to the chemoradiation therapy advances, but also in the fact that we've had surgical advances, as well as advances in minimally invasive endoscopic management of these lesions, as well. Adenocarcinoma in this country, is the most common esophageal cancer. The incidence is about 5.31 out of 100,000 cases. The risk factors are interesting. Because if you note alcohol is not a risk factor for adenocarcinoma. We do see Barrett's esophagus, GERD, or gastroesophageal reflux disease, smoking, obesity, male sex, and white race, all considered risk factors for adenocarcinoma. Another interesting point is to note that this cancer often occurs in the distal esophagus almost 75% of the time. So we cannot talk about adenocarcinoma without touching on Barrett's Esophagus first. Barrett's Esophagus is essentially replacement of the normal squamous lining of the esophagus with a more columnar intestinal tissue. What we can see endoscopically here on the right Is that you have a normal pink esophageal tissue right here. And this is the healthy squamous tissue that we should normally see. And in addition to that, you see this very sort of salmon, beefy, pink looking tissue. And that's actually columnar intestinal tissue. So it's columnar epithelialization of the esophagus. If you look on the cartoon here on the left, you see our normal GE junction would be around here and our Z line, which you can often times see in our reports is actually that junction between the normal squamous and the columnar tissue. Here you can see that the z line is not regular. Where it should normally be right here at the GE junction. You see the columnar tissue is now extending up in this irregular, sort of erratic fashion, up into where the squamous lining is. And that's why whenever we describe our Z line, if it's not at the same point as your GE junction, you know that there's Barrett's Esophagus there. So the reason we talk about Barrett's Esophagus anytime we're talking about adenocarcinoma is just like we see in colon cancer with numerous polyps progressing to cancer. We see the same thing in the esophagus. If you look on this representation, it's the British spelling of oesophagitis and esophagus. It's not a typo. You see reflux, which is one of the precursors often times for Barrett's Esophagus, resulting in inflammation. So you end up going from this very normal esophagus. But you may or may not have esophagitis. Many patients actually will present just for an EGD upper endoscopy for no reason in particular related to reflux symptoms. And you'll see that they actually have information and their completely asymptomatic or they can have reports of no information that they have ever had either history of or symptoms of, and you've see Barrett's Esophagus. So that's why the +/- oesophagitis is sort of out of the necessary algorithm but it is important to keep in mind. So we go from normal oesophagus here. There may or may not be oesophagitis. And you add this component of reflux and inflammation and you develop Barrett's Esophagus which again is the columnar intestinal epithelialization of the normal squamous esophageal tissue. Now, when you have Barrett's Esophagus, the next stage of progression is low grade dysplasia, which then progresses to high grade dysplasia, which then progresses to adenocarcinoma. Whenever we talk to patients in clinic and they present at anyone at these stages, each of them carry its on risk for adenocarcinoma. So if you see just having diagnosed of Barrett's Esophagus with no degree of dysplasia, carries about a 0.5% risk of development of adenocarcinoma. Whenever you get to low grade dysplasia, it float somewhere from between 3.5 to 8%. And high-grade dysplasia of 5% to 8%. So what are the risk factors for Barrett's Esophagus? Well age, the male gender, Caucasian ethnicity, having reflux symptoms lasting longer than ten years duration. In addition to that, if you keep in mind what we just talked about GERD, tobacco, and obesity, are risk factors for developing esophageal carcinoma. So the next cancer we'll talk about is the squamous cell carcinoma. The incidence outside the United States is 140/100,000 cases. And incident within the United States is about 3 out of every 100,000 cases. Outside the United States, esophageal cancers tend to be squamous cell carcinomas. Within the United States, it tend to be adenocarcinomas which carry with it that risk factor of obesity. And I think that relates to the obesity epidemic that we have within this country. This type of cancer can occur anywhere within the esophagus. It's male and female equal predominants. Within the United States the African-Americans have a higher risk than Caucasians. Now some of the things to keep in mind compared to the adenocarcinoma that we just talked about, males have a higher risk of developing adenocarcinoma than females. It tends to be higher risk in Caucasians, which is opposite here. And instead of happening anywhere in the esophagus, adenocarcinoma's tend to develop in the lower distal esophagus. Other risk factors for squamous cell include alcohol, also different from what we talked about before. Smoking, caustic ingestion, which include things like lye. Tylosis, which is a genetic syndrome, and is the only genetic syndrome which carries with it an increased risk of squamous cell carcinoma. It is characterized by hyperkeratosis of the palms and soles as well development of oral leukoplakia. Achalasia and dietary factors including frequent ingestion of hot beverages, n-nitrosamines, and pickled vegetables are all risk factors for squamosal development. There are other types of esophageal cancers, but they tend to be much less common. We can see sarcomas, lymphomas, carcinoids, and even melanomas. But, like I said, those tend to be rare. If you're talking about esophageal cancer, you're usually talking about esophageal adenocarcinoma and squamous cell. Now the thing about esophageal cancer, is that it is notoriously aggressive and it's for few reasons. There is direct extension into adjacent structures and through the esophageal wall. I think the fact that there's no serosal layer allows that to happen very easily as opposed to anywhere else in the body. Just like any other type of cancer, there tends to be lymphatic spread as well as hematogenous metastasis. Because you have that extensive lymphatic drainage and you have those two separate plexuses with two directions of flow. You're not only getting intra-thoracic but as well as intra-abdominal nodal spread at the same time. Now that we've reviewed the esophageal cancers and we've gone through what the esophageal wall layers are, we're going to wrap this part up and I'll see you in part two where we're going to actually go into the TN staging and we're going to see some echo-endoscopy imaging. So you have an understanding of what we actually see and how we actually stage these lesions before we go into part three where we discuss what we actually do about them.
