Workplace Violence in Health Care

Posted on June 11, 2016 by gutsandgrowth

A recent review article (JP Phillips. NEJM 2016; 374: 1661-9) discusses the topic of workplace violence against health care workers in the U.S. Fortunately, this is a topic of which I do not have any expertise. But, on reading, I was fascinated how common this occurs despite a high likelihood of being underreported and largely ignored.

For starters, there are four types of workplace violence. Type II, in which the perpetrator is a customer or patient of the workplace is thought to be most common. In hospitals, one survey indicated that this accounted for 93% of all assaults. Other types of violence include perpetrator who has no association to workplace/employee (type 1), perpetrator who is a current or former employee (type III), or a perpetrator with a personal relationship with employee, such as ex-husband (type IV).

Two areas in medicine experience the highest rates of violence: the emergency room and the psychiatry ward. In both situations, mental illness, narcotic-seeking behavior, and intoxication may play a role.

Statistics:

Nurses and nursing aides are victimized at the highest rates, likely due to increased contact time. In the Minnesota Nurses’ Study, the annual incidence of verbal and physical assaults was 39% and 13% respectively.
ER nurses had a 100% reporting verbal assault and 82.1% reporting physical assault during the previous year.
Physicians: one-quarter of ER physicians reported being the targets of physical assault in the previous year. A much higher rate of verbal threats were noted within the previous 12 months: 75%.
Weapons are used in <1% of type II episodes of violence in the health care workplace.

Solutions:

There are no clear solutions.
The author advocates not overlooking verbal threats. “The ‘broken windows’ principle, a criminal-justice theory that apathy toward low-level crimes creates a neighborhood conducive to more serious crime, also applies to workplace violence.” Addressing verbal threats may prevent escalation.
To ensure a safe environment, more reporting on this problem is needed along with investigations of potential mitigating strategies.

My take: I have had been yelled at before and I was quite shocked. This is a topic that is not discussed widely in training and probably should be.

Gibbs Gardens

False-positive Tissue Transglutaminase Antibodies

Posted on June 10, 2016 by gutsandgrowth

While tissue transglutaminase IgA antibody is thought to have high specificity for celiac disease, other etiologies need to be considered. As an example, KR Schwartz et al. (NEJM 2016; 374: 1466-76) present a case report which describes a 12 year old who was diagnosed with lymphoma after presenting with anemia, abdominal pain, and fevers. One interesting point was the elevated tissue transglutaminase IgA antibody of 74 (0-15) at presentation; endomysial antibody was negative. The TTG IgA normalized with treatment. The authors note that the presence of TTG IgA antibodies “is not specific for celiac disease but rather is a general phenomenon related to mucosal lesions.”

Related blog posts:

What to Make of a Low Alkaline Phosphatase

Posted on June 9, 2016 by gutsandgrowth

Every now and then I see a low alkaline phosphatase (ALP)–usually this is an inconsequential finding. A recent study (V Saraff et al. J Pediatr 2016; 172: 181-6) provides insight into this problem.

In a retrospective study spanning 8 years, the authors identified 1526 samples from 323,064 which had an ALP <100 U/L. Most of these were transient. Only 18 were identified as having persistently low ALP. In this group, 13 were tracked down. In this group, among four who had ongoing low ALP, two had mutations in the ALPL gene.

The authors propose, in Figure 3, how to manage a low ALP. In those with an accurate ALP (not a degraded blood sample) and who were not chronically ill, they suggest looking for symptoms of hypophosphatasia:

respiratory failure
vitamin B6 responsive seizures
elevated calcium, phosphate and/or nephrocalcinosis
failure to thrive/short stature
fractures/bone pain
craniosynostosis
chest deformity
delayed walking, waddling gait
premature loss of teeth/late dentition

In those with likely hypophosphatasia, confirm with a pyridoxal-5′-phosphate and urinary phosphoethanolamine. If these are normal, hypophosphatasia is unlikely. If these are elevated, the next step per the authors would be checking knee, lateral/AP skull. If these are suggestive, then undergoing genetic testing is recommended or seeing a bone specialist.

In those with those who do not have symptoms of hypophosphatasia, the authors recommend checking for other causes. Workup could include zinc, magnesium, thyroid function, blood counts, renal/liver assays, parathyroid hormone, vitamins B12/C/D, celiac serology, and ceruloplasmin.

My take: In those with persistently low alkaline phosphatase, keep this reference handy.

Related blog post (for high alkaline phosphatase): We still see this

Gibbs Gardens

Ozanimod for Ulcerative Colitis

Posted on June 8, 2016 by gutsandgrowth

The results of a phase 2 trial for Ozanimod have been published: WJ Sandborn et al. NEJM 2016; 374; 1754-62.

Ozanimod (RPC1063) is “an oral agonist of the sphingosine-1-phosphate receptor subtypes 1 and 5 that induces peripheral lymphocyte sequestration, potentially decreasing the number of activated lymphocytes circulating to the gastrointestinal tract.”

From the abstract:

METHODS

We conducted a double-blind, placebo-controlled phase 2 trial of ozanimod in 197 adults with moderate-to-severe ulcerative colitis. Patients were randomly assigned, in a 1:1:1 ratio, to receive ozanimod at a dose of 0.5 mg or 1 mg or placebo daily for up to 32 weeks. The Mayo Clinic score was used to measure disease activity on a scale from 0 to 12, with higher scores indicating more severe disease; subscores range from 0 to 3, with higher scores indicating more severe disease. The primary outcome was clinical remission (Mayo Clinic score ≤2, with no subscore >1) at 8 weeks.

RESULTS

The primary outcome occurred in 16% of the patients who received 1 mg of ozanimod and in 14% of those who received 0.5 mg of ozanimod, as compared with 6% of those who received placebo (P=0.048 and P=0.14, respectively, for the comparison of the two doses of ozanimod with placebo). Differences in the primary outcome between the group that received 0.5 mg of ozanimod and the placebo group were not significant; therefore, the hierarchical testing plan deemed the analyses of secondary outcomes exploratory. Clinical response (decrease in Mayo Clinic score of ≥3 points and ≥30% and decrease in rectal-bleeding subscore of ≥1 point or a subscore ≤1) at 8 weeks occurred in 57% of those receiving 1 mg of ozanimod and 54% of those receiving 0.5 mg, as compared with 37% of those receiving placebo. At week 32, the rate of clinical remission was 21% in the group that received 1 mg of ozanimod, 26% in the group that received 0.5 mg of ozanimod, and 6% in the group that received placebo; the rate of clinical response was 51%, 35%, and 20%, respectively. At week 8, absolute lymphocyte counts declined 49% from baseline in the group that received 1 mg of ozanimod and 32% from baseline in the group that received 0.5 mg. The most common adverse events overall were anemia and headache.

CONCLUSIONS

In this preliminary trial, ozanimod at a daily dose of 1 mg resulted in a slightly higher rate of clinical remission of ulcerative colitis than placebo. The trial was not large enough or of sufficiently long duration to establish clinical efficacy or assess safety. (Funded by Receptos; TOUCHSTONE ClinicalTrials.gov number, NCT01647516.)

Endoscopic Surveillance after Esophageal Atresia: Low Yield In Pediatrics

Posted on June 7, 2016 by gutsandgrowth

A recent study of patients who had undergone repair of esophageal atresia (Koivusalo et al. JPGN 2016; 62: 562-66) confirms that “routine endoscopic surveillance had limited benefit and seems unnecessary” before 15 years of age.

A retrospective review of pediatric patients with esophageal atresia (EA) from 1980-2014) identified 209 patients with 616 biopsies. 60 patients had undergone antireflux surgery. Key findings:

Gr I esophagitis was noted in 37%, Gr II or III in 16%.
Gastric metaplasia was found in 17% and reached a prevalence of 15% by age 15 years.
Only 9% of patients with gastric metaplasia and 32% of patients with gr II esophagitis were symptomatic.
No cases of dysplasia or cancer were identified.

My take: Conditions, including esophageal atresia, that predisposed to chronic reflux esophagitis increase the risk of esophageal malignancy; however, this risk remains very low in childhood. Therefore, surveillance for asymptomatic children is not needed prior to age 15 years.

Related blog post: Never quite right | gutsandgrowth

Vik Muniz recreation of Mary Cassatt painting

Up close, one sees this painting is actually a collage of images

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist. This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Extent of Disease: Microscopic or Endoscopic Classification?

Posted on June 6, 2016 by gutsandgrowth

Several recent articles highlight the divergence between microscopic and endoscopic classification of disease.

Verstraete et al. JPGN 2016; 62: 242-5.
Asthon et al. JPGN 2016; 62: 246-51.
Pashankar et al. JPGN 2016; 62: 314-16.

The first two references describe histology in comparison to endoscopic extent of disease in pediatric Crohn’s and the 3rd reference provides information on the finding of “duodenitis.”

Verstraete et al selected 60 patients randomly from their cohort for retrospective review. Two physicians independently reviewed the patients. In describing extent of disease, the extent of disease (Paris Classification) was discordant in 34 (56.6%) when comparing macroscopic disease (imaging and endoscopy) to macroscopic/microscopic combined. In addition, there was high interobserver variability of the physicians when the physicians reviewed just macroscopic findings (κ= 0.53).

Asthton et al examined data from 172 pediatric patients with inflammatory bowel disease. They found that histologic disease was more extensive than endoscopic findings. For example, among those with ileal biopsies, 49% had endoscopic findings compared with 71.3% having histologic disease.

Currently, the Paris classification relies on endoscopic findings; however, together these two studies suggest that the microscopic findings need to be considered as well. How often areas with microscopic disease will eventually develop endoscopic lesions is not clear.

Pashankar et al, reviewed pathology reports over a 5-year periods with 2772 children (mean age 10.6 years). They identified duodenitis in 352 with a prevalence rate of 12.7%. Gastritis was seen in 64% of children with duodenitis. Interestingly, 63% of the cases with histologic duodenitis had normal endoscopic appearance. Reported reasons for duodenitis:

Celiac disease 32%
Crohn’s disease 13%
Ulcerative colitis 3%
Helicobacter pylori infection 6%
Functional dyspepsia 7%

The remaining children (36%) were considered to have nonspecific duodenitis. The authors state: “this finding is similar to the high percentage of nonspecific duodenitis (60%) in adults.”

My take: It is difficult to know how important microscopic findings are in many cases. With inflammatory bowel disease, whether/how to incorporate microscopic findings in classification is unclear. With regard to the finding of microscopic duodenitis, when a specific etiology has not been identified, this leads to lots of questions:

How important is this finding?
How should this be treated?
How much additional workup and followup is needed?
How helpful is your pathologist –is the threshold for abnormality too low histologically?

Related blog posts:

What I did not know …a few items

Posted on June 5, 2016 by gutsandgrowth

6-Mercaptopurine (6-MP) often can be used when patients are intolerant of azathioprine. S Hubener et al. Clin Gastroenterol Hepatol 2016; 14: 445-53. This retrospective study showed that 15 of 20 patients with autoimmune hepatitis and prior azathioprine intolerance responded to 6-MP. This is somewhat unexpected as azathioprine is metabolized into 6-MP. However, rather than 6-thiouracil, the “imidazol component of azathioprine, which is cleaved off…might trigger adverse reactions.” Another artical on thiopurines (Aliment Pharmacol Ther 2016; 43: 863-883) (thanks to Ben God for this reference) provides a thorough review of the pharmacogenetics and pharmocokinetics of these medications. While this review reinforces the recommendation to check TPMT before treatment, it notes that only a small proportion of thiopurine toxicity is related to deficient TPMT activity.
There is no formal validated or consensus definitions of mild, moderate, or severe IBD. L Peyrin-Biroulet et al. Clin Gastroenterol Hepatol 2016; 14: 348-54. While the Lemann index measures the cumulative structural bowel disease, the authors propose criteria which involves three areas of severity: impact of the disease on the patient (eg. clinical symptoms), inflammatory burden (eg. biomarkers, mucosal disease, disease extent), and disease course (eg. structural disease, intestinal resection, perianal disease, extraintestinal manifestations)
Fundic gland polyps (often associated with proton pump inhibitor therapy) are not premalignant lesions. There is an “inverse correlation between the FGPs and gastric neoplasia.” S Varghese et al. Gastroenterol Hepatol; 2016; 12: 153-4.
Parents of newborns do not know how to use car seats. BD Hoffman et al (J Pediatr 2016; 171: 48-54) showed that 95% of car seats were misused (291 families). Serious misuse was present in 91%.

Related blog posts: Lemann index: Short Takes on IBD Articles | gutsandgrowth

Gibbs Gardens has >20 million daffodils

Mirtazapine for Functional Dyspepsia

Posted on June 4, 2016 by gutsandgrowth

In a randomized, placebo-controlled pilot study (J Tack et al. Clin Gastroenterol Hepatol 2016; 385-92) with 34 patients (29 women, median age 35.9 years), the authors showed improved dyspepsia symptom scores at weeks 4 and 8 compared with baseline.

Background: Mirtazapine is an antidepressant which is associated with weight gain and improvement in nausea.

Methods: The treatment group received 15 mg each day.

Results:

Compared with the control group, these was improvement in early satiety, quality of life, GI-specific anxiety, nutrient tolerance, and weight loss.
Two patients in the treatment group dropped out due drowsiness. Interestingly, the trend of improvement was greater at week 4 then for week 8.
The authors note that epigastric pain and burning did not improve.

Limitations: small number of patients, and tertiary care patient population

My take: more studies are needed for this vexing problem

Related blog posts:

Fountain at Gibbs Gardens

Chronic Granulomatous Disease and GI Involvement

Posted on June 3, 2016 by gutsandgrowth

Chronic granulomatous disease associated inflammatory bowel disease primarily involves the anus and rectum (SK Khangura et. al. Clin Gastroenterol Hepatol 2016; 14: 395-402). In this study from the NIH, among 78 patients with CGD-IBD enteric fisula were found in 18% (73% were perianal), colonic stictures were noted in 24% (80% in anorectal area).

Other findings:

-EGD showed inflammation in 21%, 74%, and 37% of patients in esophageal, gastric and duodenal biopsies respectively
-Small bowel disease was unusual, though two of the four patients with ileostomies had ileal ulcers
-” ‘Target-like lesions,’ which have a clear elevated center with surrounding erythema, were characteristic of mild disease
-Approximately 40% of CGD patients have GI tract involvement
-GI tract malignancy was not observed in this cohort
-24 patients had pancolitis

My take: This reference provides comprehensive details of the clinical features of a large cohort with CGD.

Which animals kill the most humans

Understanding the Risks of Propofol for Colonoscopy

Posted on June 2, 2016 by gutsandgrowth

A recent article & editorial (KJ Wernli et al. Gastroenterol 2016; 150: 888-94 & 801-2) shows that the use of propofol, delivered by an anesthetist, is associated with a small increase risk of adverse events. This finding goes against assumptions that there would be reduced complications with an anesthesia expert in the room who could manage resuscitation and airway problems.

The study analyzed claims data from more than 3 million colonoscopies in the U.S between 2008-2011 in 40-64 year-olds.

Key findings:

Use of anesthesia was associated with a 13% increase in the risk of any complications within 30 days.
The increased risk included perforation (OR 1.07), hemorrhage (OR 1.28), and abdominal pain (OR 1.07). Interestingly, the perforation risk was increased only in those undergoing polypectomy (OR 1.26) indicating that some confounders may have been difficult to eliminate.
Complications secondary to anesthesia were present as well (OR 1.15) and stroke (OR 1.04).

This is not the first study to associate anesthesia with increased risk of aspiration and mechanical complications (Cooper G et al. JAMA Intern Med 2013; 173: 551-6). It is certainly possible that the increased risk is due in part to patient selection, despite attempts to control for this.

It is also important to note that better sedation has not resulted in improved colonoscopy outcomes like increased polyp detection.

Will these results change anything? No.

The small increased safety risk (detectable only in studies of millions of patients), if accurate, is not going to stop the use of anesthesia services for two reasons.

Patient satisfaction
Financial incentives

Patient satisfaction. Propofol results in excellent sedation, often with complete absence of pain combined with rapid recovery and an antiemetic effect.

Financial incentives. Many endoscopists are able to employ an anesthetist and generate additional revenue by billing for sedation (in addition to the costs of the endoscopist), whereas this is not allowed with the combination of intravenous opioids/benzodiazepines used for ‘deep sedation.’ Even in the many who do not receive revenue for these services, the rapid recovery expedites patient care and room turnover.

My take: While propofol administered by anesthetists is a little less safe and more expensive, it is here to stay, at least until incentives are created to reconsider this approach.

Georgian Terrace