Our office has produced a new video describing “where” snoring comes from determined by a simple procedure known as sedated or sleep endoscopy. At its most basic definition, snoring is noise produced from a vibrating mucosal surface in the upper airway.
Though snoring can be defined simply, the tough question is WHERE are these vibrating mucosal surfaces? Because unless one can define WHERE the snoring is coming from, successful treatment can’t be pursued definitively.
An office exam performed while a patient is awake is suboptimal as the patient is awake… and not snoring. As such, it is an educated guess where the snoring problem is stemming from.
The right side of the colon seems to be the Achilles heel of colonoscopy because polyps there tend to be flat and harder to find, and we confer the least protection from later colon cancer in that zone.
A recent article summary in Journal Watch Gastroenterology concludes that when we see a right-sided colon polyp, we may have missed another, so we should go back and look again.
This provocative recommendation represents a major change in the way we normally perform colonoscopy. But the issue is, and always has been, how to identify and remove all polyps from the colon.
I have observed extreme variation in how my colleagues manage GI foreign-body retrieval from the stomach. Some always use general anesthesia and endotracheal intubation; others (myself included) use conscious sedation. Some use an overtube to withdraw the object into if possible; others simply pull it up to the endoscope and use the endoscope to guide it through the esophagogastric junction and upper esophageal sphincter. The reasons for this variation are clearly related to the perceived risk of airway compromise or gastrointestinal wall injury during withdrawal of the object from the stomach.
So my questions to you are:
1) When do you ask for endotracheal intubation during foreign-body retrieval?
2) Do you use an overtube when removing foreign bodies from the stomach, and, if so, always or in what situations?
3) If you don’t use an overtube, what technique do you use during withdrawal of the object?
4) What is your favorite “tool” or endoscopic accessory to grab objects from the stomach?
I look forward to hearing your thoughts on this issue.
I have noticed that we all think we are the best endoscopist around (in my case, that is indeed true!). However, we really never measured colonoscopy skill as a “patient-centered” metric and instead often use speed, efficiency, sedation needs, etc. when judging our colleagues. What is more important than these measures, however, is whether we find and remove adenomas, thereby preventing colon cancer downstream in our patients.
A number of surrogate markers for quality colonoscopy and polyp detection have been used in the past, including scope-withdrawal time from the cecum. But the one measure that has been the best predictor of quality is an endoscopist’s ADR (adenoma detection rate). In fact, this is the most reliable quality measure yet determined, and it may become the basis for being paid for these procedures in the not so distant future.
So I need to ask you:
1) Do you know your ADR?
2) Do you or does your group compare your ADR to other endoscopists within your endoscopy unit or practice?
3) Is there a program to increase ADR in low performers in your endoscopy unit?
4) Do you use your ADR as a marketing tool?
5) What is your take on the ADR as a quality measure?
If you’re from a Western country, there’s a 10-20 percent chance that you suffer from classic symptoms of acid reflux: chronic heartburn and/or acid regurgitation.
But if you don’t have those classic symptoms you may still have acid bubbling up from the stomach into the esophagus, a condition called “gastro-esophageal reflux disease” (GERD). Over the past decade, research has suggested that acid reflux can cause atypical symptoms such as cough, hoarseness, sore throat, asthma, and even chronic sinusitis. GERD can also cause chest pain, especially if the acid causes the muscle in the esophagus to go into spasm.
As an internist and gastroenterologist, I’ve seen patients who have suffered for years with atypical symptoms of GERD get better with treatment. Although I usually prescribe acid-reducing medication, I try to avoid an approach that relies exclusively on “better living through chemistry.” In fact, my goal is to treat the symptoms with life-style adjustments alone if possible. Smoking and obesity both increase acid reflux and must be addressed. I tell my patients to limit alcohol, caffeine, chocolate, peppermint, and fatty foods (I know, basically anything that gives them even an iota of pleasure in life). I also suggest keeping a food diary to try to identify culprits such as tomato-based products or certain spicy foods. If their symptoms resolve then they can try to reintroduce the things they miss the most. Elevating the head of the bed can sometimes help.
The most serious consequence of chronic acid reflux is esophageal cancer. About ten percent of patients with long-standing acid reflux develop changes in the swallowing tube that increase the risk of developing adenocarcinoma, a deadly cancer with a 5-year survival rate of less than fifteen percent. The condition is called “Barrett’s esophagus. “Fortunately, only about one in 200 patients with Barrett’s esophagus develops cancer each year. And over the last year a treatment called “radiofrequency ablation” has been found to be extremely effective in treating Barrett’s esophagus that is starting to show signs that it may turn into cancer.
It’s estimated that almost 15,000 Americans will die from esophageal cancer this year. Fifty years ago, more than 95% of esophageal cancers were “squamous cell” – the kind caused by smoking and excess alcohol use. As smoking has declined, the incidence of squamous cell carcinoma has dropped. But for reasons that are not clear, esophageal adenocarcinoma – the kind linked to acid reflux (and smoking) – has dramatically increased over the past forty years and now accounts for about half the cases of esophageal cancer. From 1975 to 2001 there was a 600 percent rise in esophageal adenocarcinoma. The obesity epidemic may well be playing a role by increasing the number of adults with acid reflux.
Gastroenterologists can diagnose acid reflux by slipping a thin, flexible instrument (endoscope) through the mouth and down the esophagus. It’s a lot easier than it sounds. Patients are usually given sedation and the back of the throat is sprayed with numbing medicine to avoid gagging. There’s no problem breathing because the tube doesn’t go into the breathing tube (the trachea). Biopsies can be taken from the last part of the esophagus to look for microscopic evidence of Barrett’s and inflammation (esophagitis) caused by acid reflux.
There is currently a controversy about who should be endoscopically screened to look for evidence of Barrett’s esophagus. Only a fraction of the millions of patients with chronic reflux will ever develop Barrett’s. And many patients with Barrett’s have no symptoms at all. In a study in Sweden, 1.6% of the population had Barrett’s but only about 40% had heartburn. And only about half of esophageal adenocarcinoma is estimated to be a result of reflux.
The American College of Gastroenterology recommends against screening the entire population but says it may be appropriate in certain populations at higher risk – such as Caucasian males over 50 with longstanding heartburn. That would be me. So for this week’s episode of CBS Doc Dot Com, I underwent an upper endoscopy, explained and performed expertly by Dr. Mark B. Pochapin, director of The Jay Monahan Center for Gastrointestinal Health at New York-Presbyterian Hospital/Weill Cornell Medical Center. For more information about the Jay Monahan Center, click here.
For information about GERD from the American Society for Gastrointestinal Endoscopy, click here.
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Our office has produced a new video describing “where” snoring comes from determined by a simple procedure known as sedated or sleep endoscopy. At its most basic definition, snoring is noise produced from a vibrating mucosal surface in the upper airway.
