January 2012 Pulmonary Journal Club

360- Review. Is it what we really need?

Lockyer JM, Clyman SG. Multisource feedback (360-degree evaluation).  In: Holmboe ES, Hawkins RE, eds. Practical Guide to the Evaluation of Clinical Competence. Philadelphia: Mosby Elseiver; 2008:75-85. (no abstract or full text available)

This month’s journal club focused not on a study but rather a review of a concept being applied in medical education-the 360-degree evaluation of clinical competence. This concept was initially developed in industry and was designed to review performance of employees in the absence of an on site supervisor.  It has been adopted in the medical community and has become an ACGME requirement in the evaluation of fellows in training. The evaluation incorporates surveyed feedback from multiple personnel with the intent to identify strengths, weaknesses and areas of concern. Personnel often include nurses, pharmacists and patients themselves. The concept is simple, the more feedback received the better a physician you can potentially become.

The strengths of the 360-degree evaluation include the following:

1. The evaluation is based on work being done
2. Constructing the survey lends insight into areas that may have otherwise been neglected.
3. Evaluations can be measured against peers

The weaknesses include:

1. No standardization on what is to be surveyed or measured
2. No way to account for bias
3. Does not measure potential
4. No Randomized controlled studies to show it improves performance

I have to admit, the 360 concept is appealing, but the caveat is limiting what is being measured. Unlike other industries medical training is constantly supervised. Medical students are supervised by interns who are supervised by residents who are supervised by fellows who answer to attending physicians. This hierarchy has existed and flourished for generations, so why is there a need to expand? Perhaps it is because physicians rate other physicians based largely on knowledge, skill sets, and clinical competence and less so on intangibles such as collaborative efforts and behavior. The 360 review does have its place, and could be a useful too if measurements are restricted to observations such as communication skills, bedside manner, response to nursing concerns, and overall professionalism. In my opinion its role is most useful as a marker of professionalism in the work place. Hopefully we do not loose sight of this and expand its role into judging clinical competency which should remain in the hands of supervising physicians.

Manoj Mathew, MD FCCP, MCCM

Reference as: Mathew M. January 2012 pulmonary journal club. 2012;4: 32. (Click here for a PDF version of the journal club)

January 2011 Pulmonary Journal Club

Austin MA, Willis KE, Walters EH, Wood-Baker R. Effect Of High Flow Oxygen On Mortality In Chronic Obstructive Pulmonary Disease Patients in prehospital setting: A Randomized Controlled Trial. BMJ 2010; 341:c5462. (Click here for abstract).

Reference as: Mathew M. January 2011 Pulmonary Journal Club. Southwest J Pulm Crit Care 2011;2:7-8. (Click here for PDF version)

It would seem that the use of oxygen in the treatment of an acute COPD exacerbation would be of obvious benefit…but how much is too much? While it’s well known that hyperoxia in COPD patients decreases minute ventilation, increases CO2 retention, and worsens respiratory acidosis, a trend to administer high flow oxygen in patients with acute COPD exacerbation still persists. The study published by Austin et al, is an unblinded randomized controlled trial evaluating 2 parallel groups treated during the prehospital phase of their acute COPD exacerbation. Patients were randomized to receive either high flow oxygen at 8-10 L/min via a nonrebreather mask –vs- titrated oxygen flow to keep oxygen saturations between 88-92%. Patients in both groups also received standard treatment with salbutamol, ipatroprium, and dexamethasone. The primary outcome was prehospital and in hospital mortality. A total of 62 patients met final inclusion criteria; 30 in the control arm, and 32 in the oxygen titration arm. The results demonstrated that treatment with high flow oxygen was associated with higher mortality with a number needed to harm of 1:14. However the key element to qualify this conclusion was missing. An ABG to confirm the presence and severity of respiratory acidosis in the setting of hyperoxia was recorded in only 11% of the patients. Perhaps a venous blood gas measurement in the prehospital setting would have assisted in directing level of oxygen delivery with regards to severity of acidosis. Although this study does support data known from prior studies a conclusive stand on this clinical dilemma remains to be set. Even in our own academic institution we struggle with the dogma that COPD patients need to have oxygen saturations that exceed 92%. With the current level of evidence we do know that oxygen saturations may need to titrated and high flow oxygen is probably harmful in chronic COPD patients

Prepared by Manoj Mathew, MD

December 2011 Pulmonary/Sleep Journal Club

Reference as: Mathew M. December 2011 pulmonary/sleep journal club. Soutwest J Pulm Crit Care 2011;3:171. (Click here for PDF version of the journal club)

Cano-Pumarega I, Durán-Cantolla J, Aizpuru F, Miranda-Serrano E, Rubio R, Martínez-Null C, de Miguel J, Egea C, Cancelo L, Alvarez A, Fernández-Bolaños M, Barbé F. Obstructive sleep apnea and systemic hypertension: longitudinal study in the general population: the vitoria sleep cohort. Am J Respir Crit Care Med 2011;184:1299-304. (Click here for abstract)

Obstructive Sleep Apnea (OSA) is a disorder characterized by intermittent episodes of apnea/hypopnea in which there are periodic oxygen desaturations. These episodes may also result in tachycardia, bradycardia and other EKG abnormalities. The prevalence of OSA per the Wisconsin cohort Study is reported as 4-9% for women and 9-24% for men. There is also an increased prevalence in age groups > 65.  Prior observational studies have shown increased cardiovascular mortality from acute MI, stroke and sudden cardiac death from untreated severe OSA. The link between OSA and the development systemic hypertension has also been postulated. Prior Observational Studies (Wisconsin Sleep Cohort Study, Sleep Heart Health Study) demonstrated discordant results with a positive association seen only in the Wisconsin Sleep Cohort Study. This study was done to see if the diagnosis of OSA serves as an independent risk factor in the development of systemic hypertension.

This study was an observational cohort study done in Spain over 2 phases. Patients were excluded if they were on CPAP, had a known diagnosis of systemic hypertension or had undergone an uvulopalatopharyngoplasty.  2148 pts were eligible for the study and a total of 1557 pts completed the study. The patients with a diagnosis of OSA and no prior diagnosis of systemic hypertension were followed over 7-8 years. The results did not show an increased incidence of systemic hypertension in patients with OSA when other variables such as age, gender, fitness level, BMI, and neck circumference were accounted for.

The study was well done and supported the results of The Sleep Heart Health Study.  The strengths of the study were its large sample size and its design. Although there may not be a causal relationship between OSA leading to systemic hypertension, we can not deny the prevalence of hypertension in patients with OSA. From a clinical standpoint I would like to have another question answered.....should patients with newly diagnosed hypertension or multiple drug resistant hypertension undergo screening for obstructive sleep apnea?

Manoj Mathew, MD MCCM, FCCP

Associate Editor

Pulmonary Journal Club

October, 2011 Pulmonary Journal Club

Reference as: Zaner R, Mathew M. October, 2011 pulmonary journal club. Southwest J Pulm Crit Care 2011;3:87-89. (Click here for a PDF version)

Albert RK, Connett J, Bailey WC, Casaburi R, Cooper JA Jr, Criner GJ, Curtis JL, Dransfield MT, Han MK, Lazarus SC, Make B, Marchetti N, Martinez FJ, Madinger NE, McEvoy C, Niewoehner DE, Porsasz J, Price CS, Reilly J, Scanlon PD, Sciurba FC, Scharf SM, Washko GR, Woodruff PG, Anthonisen NR; COPD Clinical Research Network. Azithromycin for prevention of exacerbations of COPD. N Engl J Med 2011;365:689-98. (Click here for abstract)

Chronic obstructive pulmonary disorder, COPD, has a prevalence of approximately 10% in people over the age of 40 and an estimated 24 million adults in the United States suffer from symptoms of COPD. Acute exacerbations of chronic obstructive pulmonary disease result in an increased risk of death, decreased quality of life, and a more rapid decline in lung function than those patients with COPD who do not suffer from exacerbations.

This study was a randomized trial that recruited patients from 17 different sites to determine whether daily azithromycin decreased the frequency of acute exacerbations in patients with COPD. The study was a prospective, parallel-group, placebo-controlled trial that took place from March 2006 through June 2010. There were 1142 participants, 570 in the azithromycin group and 572 in the placebo group. Participants in the azithromycin group were to take 250mg by mouth daily for one year; participants in the placebo group also took a similar appearing tablet for one year.

Participants in both groups were at least 40 years of age, had a clinical diagnosis of COPD confirmed by pulmonary function testing, had received systemic glucocorticoids within the previous year, or used continuous supplemental oxygen, or had gone to the emergency department or been admitted to the hospital for an acute COPD exacerbation. The participants were not included in the study if they had an acute exacerbation within four weeks prior to joining the study. Participants were excluded from the study if they had asthma, a resting heart rate greater than 100 beats per minute, a prolonged QT interval (>450msec), hearing impairment confirmed by audiometric testing, or were also using drugs that could prolong the QT interval or were associated with torsades, with the exception of amiodarone. The breakdown of participants had approximately 26% at GOLD stage II, 40% GOLD stage III, and 34% GOLD stage IV at the time of the study in both the placebo and azithromycin groups.

Primary outcome of the study was the time to the first acute COPD exacerbation, which was defined as: increased or new onset of either cough, sputum, wheezing, chest tightness or dyspnea of at least three days requiring antibiotics or systemic steroids. The date of the exacerbation was documented via clinic visit or telephone contact and was recorded as the date treatment was prescribed.

Secondary outcomes of the study were quality of life determined by two different questionnaires, nasopharyngeal colonization of Staphylococcus aureus, Streptococcus pneumonia, Haemophilus influenza or Moraxella, and adherence to the drug regimen. Nasal swabs were done at enrollment and every three months during the study looking for colonization and macrolide resistant bacteria.

Results of the study showed 1641 acute COPD exacerbations, 741 in the azithromycin group and 900 in the placebo group. There was a significant difference in the time to first exacerbation between the two groups with a median time to the first exacerbation of 266 days in the azithromycin group and 174 days in the placebo group. Frequency of exacerbations was found to be significantly lower in the azithromycin group and the number needed to treat to prevent one exacerbation would be approximately three patients.

Secondary outcomes, however, had less significance. Although statistically significant improved quality of life per questionnaire the group did not meet the minimum goal they had set prior to the start of the study to establish improved quality of life. There proved to be no significant difference in the rate of adherence to azithromycin compared to placebo. There was an increase in hearing deficits in the azithromycin group by 5% when compared with placebo. Unfortunately all patients who suffered a hearing deficit were to be taken off azithromycin immediately, which did not occur in all patients due to a protocol error. There was also no significant difference seen in the rate of death between the two groups, which demonstrated three percent in the azithromycin group and four percent in the placebo group.

Regarding colonization of organisms in the nasopharynx, those patients not colonized at the beginning of the study who were placed on azithromycin had a decreased incidence of new colonization compared to those on placebo, and this was found to be significant with a P <0.001. However, in those people without colonization prior to the study who then became colonized during the study there was an increase in resistance to macrolides versus the placebo group, (81 percent vs. 41 percent) and this was also significant. However, there was no evidence showing that the exacerbations occurring in the azithromycin group were due to the new macrolide resistant bacteria. Those people already colonized prior to the study had no significant difference in the prevalence of resistance to macrolides, but this finding was not statistically significant.

The data from this study looks promising. We know that macrolides have immune modulatory and anti-inflammatory effects in addition to antibacterial effects, the former of which are likely offering much of the benefit observed in this study. However, it is still too soon to say that this should become the next step in preventing COPD exacerbations. Azithromycin is used in cystic fibrosis patients with bronchiectasis 500 mg by mouth three times a week to help prevent exacerbations, but we also see an increase in multidrug resistant bacteria in that population. This study does not follow patients long enough out to see if a similar result will occur with COPD. A larger study with longer follow up targeting GOLD stage III and IV participants already on appropriate medical management may be of benefit. In this study it was difficult to tell if those participants involved were already on appropriate medical management and receiving standard of care and if not would there have been similar results from implementing that without the risk of worsening macrolide resistance. That being said, for my own patient population, I would consider using azithromycin for COPD exacerbation prophylaxis in the patient that is suffering from severe disability from repeat COPD exacerbations, is already on optimal medical management and even on optimal management is still requiring frequent hospitalizations for acute exacerbations of COPD.

Rebecca Zaner, D.O.

Manoj Mathew MD, FCCP, MCCM

Associate Editor, Pulmonary Journal Club

September, 2011 Pulmonary Journal Club

Reference as: Mathew M. September, 2011 pulmonary journal club. Southwest J Pulm Crit Care 2011;3:70-1. (Click here for a PDF version)

Rahman NM, Maskell NA, West A. Intrapleural use of tissue plasminogen activator and DNAse in pleural infection. N Engl J Med 2011;365:518-26. (Click here for article abstract)

The use of intrapleural fibrinolytics in the management of pleural space infections and loculated effusions has been in contestation for nearly 20 years. In 2004 a Cochrane review of the 4 Randomized controlled trials demonstrated a potential benefit of intrapleural streptokinase therapy vs. placebo in the management of pleural space infections and loculated effusions. The follow up study …Multicenter Intrapleural Sepsis Trial (MIST1) was supposed to answer the question on the efficacy intrapleural fibrinolytic therapy but its results were discordant with prior data, showing NO benefit of streptokinase compared to placebo in reducing hospital days, surgical referrals, or mortality.  The discordant results have been challenged on various levels including time to therapy (which was 14 days), and subjective radiographic criteria in enrollment.  The study also questioned the pathophysiology behind failure of fibrinolytic monotherapy and whether an additional agent to promote DNA cleavage is needed. The study looks to compare the efficacy of combination therapy of TPA + DNase vs. Placebo vs. TPA or DNase as monotherapy.

The study was a double-blinded, randomized, controlled trial performed at 11 centers in the United Kingdom. Inclusion criteria were clinical evidence of infection and pleural fluid showing any one of the following: positive culture, purulence, pH< 7.2 or a positive gram stain. A total of 210 pts were enrolled and received either placebo (55 pts), TPA (52 pts), DNase (51 pts) or TPA + DNase (52 pts). Treatment was given as twice daily pleural instillations for 3 days. The primary outcome was a radiographic change in pleural opacity on day 7 vs. day 1. Secondary outcomes looked at rates of surgical referral, length of hospital days, and volume of fluid drained by day 7.

The results showed the that  combination therapy with TPA + DNase showed a decrease in pleural opacity, decreased surgical referral (4% vs. 14% in placebo) and decrease in hospital days by 6.7 days when compared to placebo.  Monotherapy with either TPA or DNase showed no benefit when compared to placebo.

Our review of the study showed that it was well done and prompted a discussion on our own experiences. Several of our faculty has noted marked clinical and radiographic response when using TPA or Streptokinase as monotherapy, myself included.  The development of loculations within the plural space occurs as early as 72 hours so the duration to the first dose of intrapleural treatment at 14 days remains questionable and may explain the failure of fibrinolytic therapy in MIST 1 as well as in this study.   The study did reinforce several beliefs. First, chest tube drainage as stand alone therapy may become obsolete in the management of pleural space infection; second, the time to drainage is still beyond what is pathophysiologically sound; and finally, the use of intrapleural therapy has not been associated with significant adverse events.  Whether chest tube drainage + TPA + DNase will become the new gold standard in the management of pleural space infections is doubtful, however, it is conceivable that this may now become first line therapy especially in higher surgical risk patients.

Manoj Mathew MD, FCCP, MCCM

Associate Editor, Pulmonary Journal Club