Specialties & Topics
- Arthritis/Rheumatic Disease
- Breast Cancer
- GERD/Peptic Ulcers
July 16th, 2013
We have shifted the paradigm of treating neoplastic Barrett esophagus (BE) away from a choice between intensive surveillance or surgery and towards endoscopic ablation. In the last 5 years, I have done hundreds of BE ablations using radiofrequency ablation (RFA) and endoscopic mucosal resection (EMR), and many thousands have been performed worldwide. However, on post-ablation surveillance, evidence is lacking on whether and when patients can be cut loose. Moreover, I am beginning to see patients who were believed to be cured after ablation (no signs of BE or neoplasia during years of surveillance) showing up with adenocarcinoma in the distal esophagus 4 or more years later.
Until now, I have been telling my patients that once they are BE- and dysplasia-free, I want them to undergo surveillance every 4 months for 1 year, then every 6 months for 1 year, then yearly for a couple of years, and then every other year if things remain stable.
But given the uncertainties I’ve outlined above, I am interested in discussing your practices and recommendations for surveillance after ablation for BE.
On that note, what would your approach be in the following cases?
1) If a patient with high-grade dysplasia has their BE completely ablated (no BE and no dysplasia), what surveillance period do you recommend for the following year? Year two? Beyond 2 years?
2) If a patient with low-grade dysplasia has their BE completely ablated (no BE and no dysplasia), what surveillance period do you recommend for the following year? Year two? Beyond 2 years?
3) If a patient with NO dysplasia has their BE completely ablated (no BE and no dysplasia), what surveillance period do you recommend for the following year? Year two? Beyond 2 years?
4) Do you ever tell patients that they are cured and no longer need surveillance (e.g., after 5 years, after 10 years, etc.)?
5) If a patient with dysplasia has their neoplastic BE completely ablated (no dysplasia but residual BE), what surveillance period do you recommend for the following year? Year two? Beyond 2 years?
Please join the discussion to shed some light on this issue.
June 28th, 2013
There are innumerable bowel preps on the market as well as “home brewed” ones (e.g. Miralax™ and Gatorade™). In my community, many gastroenterology practices appear to choose their colonoscopy prep based on patient acceptability and/or taste preference. I find this choice of bowel prep based on “marketing” to patients troublesome.
Although I absolutely understand the issues of patient satisfaction (I have had two colonoscopy preps), the reality is that the quality of the bowel prep directly correlates with detection of polyps and, thus, ultimately affects the ability of colonoscopy to protect against colon cancer.
In my experience, if patients are given the choice between a bowel prep that tastes good or is easier to use and the “best” one for cleaning the colon (a split-dose, PEG-based prep) and optimizing polyp detection, they will choose the latter. Frankly, I think that the use of any less optimal prep should be accompanied with documentation that the patient is aware of the “risk” associated with use of the alternate prep (missed polyps, possible increased risk for later cancer, need for another colonoscopy earlier than usual, etc.)
So, what is your approach to this issue? Specifically, I am wondering the following:
1) How do you choose bowel preps in your practice?
2) If you choose anything other than split-dose, PEG-based preps, do you inform patients that they may have a greater risk for missed polyps?
3) Do you track bowel prep quality as a quality measure in your practice?
4) In patients with a suboptimal prep, when do you reschedule them back?
I look forward to the conversation.
June 4th, 2013
Most gastroenterologists I know seem pretty confident that they can differentiate bright red blood from a lower GI (e.g., colonic) source and massive upper GI bleeding presenting as bright red blood in the lower GI tract. The location of bleeding is critical from a treatment and prognosis perspective. Lower GI bleeding usually ceases spontaneously, requires no pharmacological intervention and rarely requires an endoscopic intervention, whereas with upper GI bleeding, PPI infusion and endoscopic therapy offer improvement in outcomes.
Because the distinction is important, some authorities suggest consideration of an urgent EGD in this situation and an elective colonoscopy (if at all). My observation is that most endoscopists do not follow this management approach: They forego the EGD and do an urgent colonoscopy.
So, let’s discuss a hypothetical case.
A patient has an apparent lower GI bleed and is hemodynamically stable upon resuscitation. Which would you do?
1. An urgent colonoscopy
2. An urgent colonoscopy, followed by an EGD if nothing is found
3. An urgent EGD and elective colonoscopy
4. Another approach
Please share your approach and the thinking behind your management strategy. I look forward to a dialogue.
April 10th, 2013
The effectiveness of endoscopic ablation of neoplastic (dysplastic) Barrett esophagus (BE) has made it the new standard of care in many communities; referrals to surgeons have largely disappeared. However, the procedure is still evolving — from thermal ablation by laser in the 1980s and early 1990s to BICAP probes and Argon Plasma Catheter (APC) in the mid-to-late 1990s to specific radiofreqency catheters (Barrx Halo 360 and 90 systems) in the current decade. Cryoablation catheters are also now available.
At the same time, endoscopic mucosal resection (EMR) technique has also evolved with the Duette and other systems. EMR now allows “wide area” resection of flat BE as well as the original approach of targeted resection of mucosal nodules and depressions.
So, with such a large variety of effective techniques available for treating limited flat BE mucosa, let me present a case study and ask what you would do.
A patient has 2 cm of circumferential BE with a single 1-cm tongue extension. Biopsies demonstrate focal high-grade dysplasia and widespread low-grade dysplasia. Careful inspection with high-definition, white-light and narrow-band imaging reveals no surface irregularity and minimal vascular heterogeneity.
- Which endoscopic technique would you use to initially treat this patient’s BE? Why?
- Which technique would you use in follow-up sessions? Why?
- How much of the BE would you treat at the first session?
- Would you treat circumferentially or the entire segment?
- How many weeks apart would you conduct treatment sessions?
I look forward to the discussion.
February 10th, 2013
In treating patients with constipation, we have several options for first-line agents: bulking agents/fiber, osmotic laxatives, or stimulant laxatives. When a patient has a suboptimal result, we commonly add or move to another class of laxative agents. Fortunately, most patients respond to these interventions, but we all have patients whose condition is “refractory” to these commonly used treatments. In the last few years, newer agents to manage constipation such as lubiprostone and linaclotide have also become available. But how best to manage these patients remains unclear, at least to me. So, here’s what I would like to know from you.
What do you use as first-line treatment in a patient with constipation?
What is your add-on treatment when your first-line treatment fails?
Do you use the newer agents, and if so, when? Do you use them to substitute for another agent or add them on?
In what circumstances do you consider surgery to treat constipation?
If a colonoscopy is negative, do you routinely use other diagnostic tests in a patient with constipation?
Looking forward to hearing your management strategies.
December 30th, 2012
Colonoscopy prevents most colorectal cancers, but only when it is performed as part of a high-quality examination. The quality measures most often discussed include cecal intubation rate, cecal withdrawal time, documentation of bowel prep quality in endoscopy reports, adenoma detection rate (ADR), and appropriate recommendation of subsequent screening or surveillance intervals after colonoscopy. While third-party payers are increasingly considering using some of the above as pay-for-performance measures, I have also noticed many more patients asking about some of these measures when they are being consented for a colonoscopy. This leads me to ask you the following.
1) Do you routinely inform your patients of your ADR, cecal intubation rate, and/or withdrawal time?
2) Do you follow guidelines regarding repeat colonoscopy intervals (i.e., 10 years for normal-risk patients with a normal exam, 5-10 years for 1-2 small adenomas, etc.)?
3) Do you document bowel prep quality on your reports, and if so, do you use a validated method such as the Boston Bowel prep score?
4) Are these above measures available on your website or posted in your office?
5) For those of you who do not do some or all of the above, why don’t you?
6) Do you think patients care about these facts?
I am looking forward to an interesting conversation.
November 11th, 2012
The diagnosis of this increasing and now epidemic infection has been evolving as well. When I first started testing for this infection, a cytotoxin assay was used that delayed the diagnosis and was very operator-dependent. Enzyme immunoassays came next, and more recently PCR testing of stool has become available. Despite the increased accuracy and more rapid results available today with PCR testing, it seems that we have not yet altered our testing pattern. It used to be that we recommended 3 separate stool samples be tested before excluding the diagnosis of C. diff infection. I know that practice remains prevalent today.
So, what I would like to find out from you are the following…
1) Do you know what C. diff test is used where you practice?
2) How quickly do you get the results back?
3) How many stool samples do you routinely test?
4) If testing is negative and symptoms persist, how long do you wait before “retesting?”
Looking forward to the dialogue.
October 10th, 2012
I am amazed at the variation I have seen in the use of endoscopic ultrasound (EUS) in staging Barrett esophagus (BE). Some of us use EUS universally, and others (myself included) never use it to stage intramucosal carcinoma or high-grade dysplasia.
So, let me propose a case and ask what you would do: The patient is a healthy 58-year-old man with 3 cm of BE with a 0.5 cm nodule in the distal segment. There is no ulceration or other surface irregularity found upon inspection with high-definition white-light and narrow-band imaging.
1) Stage with EUS and resect the nodule?
2) Resect the nodule and stage with EUS only if intramucosal carcinoma or greater neoplasia is seen?
3) Resect the nodule and stage with EUS for invasive adenocarcinoma only?
4) Perform radiofrequency ablation (RFA) of the nodule after staging EUS?
5) Perform RFA of the nodule without staging EUS?
I look forward to your comments.
August 29th, 2012
Our hospital used to provide hydrogen breath testing for the community but recently discontinued this practice. I was asked to comment on whether it should be discontinued and how often I used the test. It surprised me that I had not ordered a hydrogen breath test in the 2 decades I have been here but that many docs did. Although all of us are aware that small intestinal bacterial overgrowth can occur (e.g., scleroderma-type bowel motility disorders, post-operative blind loops, etc.), it seems that this diagnosis is being made more often in otherwise normal people without an obvious etiology.
So the conversation I want to generate is the following:
1) How often do you entertain a diagnosis of SIBO, and what symptoms/settings make you consider the diagnosis?
2) Do you think SIBO is being overdiagnosed or underdiagnosed?
3) If you consider SIBO, do you do a diagnostic test, and, if so, which one?
4) Given that no test for SIBO is validated against a gold-standard diagnosis, how do you chose the test you are using?
5) If you do not test for bacterial overgrowth, do you treat empirically, and, if so, with what?
6) What test characteristics do you want to see before you would use a test for bacterial overgrowth?
I look forward to the conversation!
August 5th, 2012
I have been using PPIs to manage GERD and acid-sensitive dyspepsia since omeprazole first became available in 1989. Although no drug class is absolutely safe, there is, as yet, not a single case report of a death related to this drug class, despite hundreds of millions of patient-years of exposure. Despite this remarkable safety profile, much attention has focused recently on the overall safety of PPIs, as they have been associated with enteric infections (e.g., c. difficile), decreased bone density, electrolyte abnormalities (e.g., low magnesium), etc. However, most of these risks have been described in epidemiological studies that can establish association but not causation, and we learned an important lesson about interpreting such results with caution after authors and the FDA sent a message about the so-called interaction between PPIs and clopidogrel that turned out to be clinically irrelevant.
Despite the benefits of PPIs, increased scrutiny of the safety of this drug class has led a number of my patients to question recommendations about trying or continuing PPI therapy. I think that patients are wise to ask about the relevant side effects of any drug, but I have had trouble giving much in the way of advice or information about PPI risks, given the lack of credible evidence of cause and effect.
So, what do you tell your patients about risks when you start them on a PPI therapy?
What do you tell patients on long-term PPI therapy?
Do you use drug holidays?
Do you do bone-density studies earlier or more often in patients on PPIs?
Do you monitor magnesium levels?
Do you have patients stop therapy if they at risk for enteric infections (e.g., from hospital antibiotic exposure, travel to developing nations, etc.)?
I am looking forward to your insightful comments.