A 'Wake- up Call' for Burnout; More From WCOG at ACG 2017

Hello. I'm Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

I'm back from the American College of Gastroenterology (ACG) annual meeting, this time in conjunction with the World Congress of Gastroenterology (WCOG). A tremendous amount of energy and enthusiasm went into this conference, which was held in Orlando, Florida, with over 6000 registrants and attendees. Hats off to ACG immediate past president Dr Carol Burke and WCOG president Dr David Bjorkman for putting together a fantastic meeting.

I want to discuss practice-changing things I took away from the conference, somewhat artificially broken up by parts of the gastrointestinal tract. Let's get started with part 1 of my takeaways.

Burnout in Gastroenterologists

A survey of burnout in gastroenterologists was a wake-up call. Dr Carol Burke and colleagues^[1] mailed a 60-item survey to ACG members in 2014-2015 to assess burnout. The Maslach Burnout Inventory, a validated instrument, was used to measure subscales of emotional exhaustion and depersonalization. Burnout was defined as scoring high in both of these categories.

While only 9.2% of surveys were returned, nearly half of the 750 or so respondents reported burnout. Drivers of burnout included the unfriendly electronic medical record (EMR), practice regulations, and maintenance of certification (MOC). (Dr Burke made MOC a priority for her administration, and we were pleased to see Dr Irving Pike, the new ACG president, acknowledge MOC as a primary concern for all gastroenterologists.)

Registrants found declining reimbursement and time spent at home related to work and domestic chores to be problems. Unfortunately, a large proportion of the respondents reported a desire to retire or leave their practice.

We need to take this as a wake-up call. I'm not sure that this is unique to gastroenterology. Some institutions are developing physician wellness programs and physician wellness initiatives to promote what we view as a potential real problem—not just for our specialty but for physicians in general.

Bariatric Surgery and Alcohol Abuse

Many bariatric surgeons counsel and monitor their patients. If not, we monitor these patients regularly for things like vitamin and mineral deficiency. I tell my patients that it's a life-long commitment, and if a surgeon is not going to do it, then we need to do this.

An interesting meta-analysis from Boston^[2] looked at the risk for alcohol abuse after bariatric surgery. The investigators found that new-onset alcohol abuse was 8% greater after bariatric surgery than otherwise would have been expected. The odds ratio of significant alcohol abuse was increased by about 50% after bariatric surgery.

We provide marital counseling in our comprehensive bariatric program because marital discourse may contribute to why these people resort to alcohol.

You need to monitor your bariatric patients for this and ask focused questions relating to alcohol abuse postoperatively.

Esophagus: Cancer in Barrett Esophagus; Opiates and Esophageal Motility

Let's turn now to the esophagus.

There was a very interesting multicenter outcomes study^[3] about missed interval cancer rates at the time of the index endoscopy in patients with Barrett esophagus (BE). The study looked at rates of missed low- and high-grade dysplasia and esophageal adenocarcinoma in nearly 3100 patients with BE who underwent at least one endoscopy after the initial diagnosis. The interval cancer rate was around 0.9%. The miss rate in those who were diagnosed with high-grade dysplasia in the first year was 3% and the miss rate for low-grade dysplasia was 10%. This suggests that a repeat endoscopy at 1 year may be more warranted than what was previously ascribed in current guidelines.^[4] For how we currently do blind biopsies, the Seattle protocol certainly leaves us a bit in abeyance; for field biopsies, the WATS^3D biopsy may be very helpful.^[5] My personal bias is to oversample the proximal esophagus, which is where you see most of the dysplasia in these patients. Again, consider a low threshold for repeat endoscopies—maybe repeat in a year.

Studies have shown that opiates can cause spastic esophageal dysmotility. You should not read a diagnosis of spastic dysmotility (eg, achalasia type III or jackhammer esophagus) if patients are on opiates.^[6] These need to be called out. We recommend not doing motility testing on patients who are on opiates. A study from the Cleveland Clinic^[7] looked at 177 patients, 18.5% or so who were taking opiates. This is very reflective of the current crisis in the United States. They found that active opiate users had higher lower esophageal sphincter and integrated relaxation pressures. Results of esophageal motility testing are interpreted as if patients are not on opiates. Do not make discriminate recommendations based on findings until patients who are on opiates are tested off opiates.

Stomach: G-POEM

Next is the stomach.

We have seen a tremendous amount of enthusiasm relating to gastric peroral endoscopic pyloromyotomy, or G-POEM, for achalasia in the endoscopic world.

A study coordinated by the group at Emory^[8] looked at G-POEM in 30 patients with refractory gastroparesis presenting with nausea, vomiting, or early satiety. It was successful in all of the patients. Patients showed significant improvements in overall quality of life, which were sustained throughout the 18-month period of follow-up. Patients also had decreased utilization of healthcare resources. G-POEM did not work as well if the predominant symptoms were bloating and pain. So, if you are looking to refer a patient to an expert center, look at the composite of the symptoms that you are referring for.

Liver: NAFLD, Hepatic Encephalopathy

Let's turn to the liver.

The topic of fibrosis in nonalcoholic fatty liver disease (NAFLD) is exploding. A single center in Mexico^[9] performed a case-controlled analysis of cardiovascular (CV) outcomes in asymptomatic patients with NAFLD. Cardiovascular risk was estimated using the American College of Cardiology/American Heart Association risk equation in conjunction with the Framingham risk score. NAFLD fibrosis scores were stratified by degree of progression: F0-F2, indeterminate; and F3-F4, fibrosis. F3-F4 patients tended to have a very strong high CV risk, with an odds ratio of nearly 10. With NAFLD, look hard at F3-F4 patients. Be aware of their CV risk, and perhaps notify your primary team that these patients are at significantly increased risk for CV disease.

The other aspect of fatty liver is, how do we predict what they truly have if we do not have a liver biopsy? The Cleveland Clinic and the Texas Liver Institute in San Antonio^[10] calculated composite noninvasive fibrosis tests (AST/ALT ratio, AST to platelet ratio index [APRI], FIB-4 index, and the NAFLD fibrosis score) in patients who had had a liver biopsy. Specificities were all in excess of 70%, but sensitivities were really pretty atrocious: AST/ALT ratio, 27%; APRI, 16.5%; FIB-4 index, 6.7%; and NAFLD fibrosis score, 44%. So we have reasonable specificity but poor sensitivity. We clearly need other ways to assess advanced fibrosis in NAFLD.

Next was the evaluation of rifaximin monotherapy for preventing recurrence of overt hepatic encephalopathy.^[11] When patients are on lactulose and rifaximin, I am asked, "Do I really need the lactulose? It's a pain and I don't like the taste of it. It gives me a lot of gas bloat." In this study, patients with cirrhosis who had one episode of overt hepatic encephalopathy, but were now in remission (Conn score ≤ 1), were randomized to rifaximin 550 mg twice daily or to rifaximin 500 mg twice daily plus lactulose. Treatment was self-titrated to achieve two to three soft stools a day for 6 months. Patients were monitored monthly for breakthrough of hepatic encephalopathy, defined by Conn score ≥ 2. Lo and behold, they found that rifaximin monotherapy was less effective than combination therapy. So, stick to your guns when patients ask whether they can come off of lactulose. The answer is no.

That wraps up the first part of what I took back from ACG. Next will be advances in the small bowel, colon, and pancreaticobiliary disease. Thanks again for listening.

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