Sunday, November 30, 2014
VA physician and staff satisfaction with performance measures
From a recent JGIM study:
The VA is a stellar health system in the artificial world of metrics.
OBJECTIVE:
To describe primary care staff (clinicians and other staff) experiences with the use of performance metrics during the implementation of the Veterans Health Administration's (VHA) Patient Aligned Care Team (PACT) model of care...
PARTICIPANTS:
Two hundred and forty-one of 337 (72 %) identified primary care clinic staff in PACT team and clinic administrative/other roles, from 15 VHA clinics in Oregon and Washington...
KEY RESULTS:
Primary care staff perceived that performance metrics: 1) led to delivery changes that were not always aligned with PACT principles, 2) did not accurately reflect patient-priorities, 3) represented an opportunity cost, 4) were imposed with little communication or transparency, and 5) were not well-adapted to team-based care.
CONCLUSIONS:
Primary care staff perceived responding to performance metrics as time-consuming and not consistently aligned with PACT principles of care. The gaps between the theory and reality of performance metric implementation highlighted by PACT team members are important to consider as the medical home model is more widely implemented.
The VA is a stellar health system in the artificial world of metrics.
Non cardiac surgery after stroke and time course of increased risk
From a recently published Danish nationwide cohort study:
Main Outcomes and Measures Risk of major adverse cardiovascular events (MACE; including ischemic stroke, acute myocardial infarction, and cardiovascular mortality) and all-cause mortality up to 30 days after surgery. Odds ratios (ORs) were calculated by multivariable logistic regression models.
Results Crude incidence rates of MACE among patients with (n = 7137) and without (n = 474 046) prior stroke were 54.4 (95% CI, 49.1-59.9) vs 4.1 (95% CI, 3.9-4.2) per 1000 patients. Compared with patients without stroke, ORs for MACE were 14.23 (95% CI, 11.61-17.45) for stroke less than 3 months prior to surgery, 4.85 (95% CI, 3.32-7.08) for stroke 3 to less than 6 months prior, 3.04 (95% CI, 2.13-4.34) for stroke 6 to less than 12 months prior, and 2.47 (95% CI, 2.07-2.95) for stroke 12 months or more prior. MACE risks were at least as high for low-risk (OR, 9.96; 95% CI, 5.49-18.07 for stroke less than 3 months) and intermediate-risk (OR, 17.12; 95% CI, 13.68-21.42 for stroke less than 3 months) surgery compared with high-risk surgery (OR, 2.97; 95% CI, 0.98-9.01 for stroke less than 3 months) (P = .003 for interaction). Similar patterns were found for 30-day mortality: ORs were 3.07 (95% CI, 2.30-4.09) for stroke less than 3 months prior, 1.97 (95% CI, 1.22-3.19) for stroke 3 to less than 6 months prior, 1.45 (95% CI, 0.95-2.20) for stroke 6 to less than 12 months prior, and 1.46 (95% CI, 1.21-1.77) for stroke 12 months or more prior to surgery compared with patients without stroke. Cubic regression splines performed on the stroke subgroup supported that risk leveled off after 9 months.
Conclusions and Relevance A history of stroke was associated with adverse outcomes following surgery, in particular if time between stroke and surgery was less than 9 months. After 9 months, the associated risk appeared stable yet still increased compared with patients with no stroke. The time dependency of risk may warrant attention in future guidelines.
Saturday, November 29, 2014
Maintenance of certification (MOC): a focus group study of physicians' perceptions
Published in JAMA Internal Medicine:
At present, MOC is perceived by physicians as an inefficient and logistically difficult activity for learning or assessment, often irrelevant to practice, and of little benefit to physicians, patients, or society.
Perioperative atrial fibrillation and long term stroke risk
Perioperative a fib is often transient and considered benign. But a recent study from a large claims database suggests a long term stroke risk:
We have no way of knowing the duration of a fib in these patients but, likely, many episodes were transient.
Main Outcomes and Measures Previously validated diagnosis codes were used to identify ischemic strokes after discharge from the index hospitalization for surgery. The primary predictor variable was atrial fibrillation newly diagnosed during the index hospitalization, as defined by previously validated present-on-admission codes. Patients were censored at postdischarge emergency department encounters or hospitalizations with a recorded diagnosis of atrial fibrillation.
Results Of 1 729 360 eligible patients, 24 711 (1.43%; 95% CI, 1.41%-1.45%) had new-onset perioperative atrial fibrillation during the index hospitalization and 13 952 (0.81%; 95% CI, 0.79%-0.82%) experienced a stroke after discharge. At 1 year after hospitalization for cardiac surgery, cumulative rates of stroke were 0.99% (95% CI, 0.81%-1.20%) in those with perioperative atrial fibrillation and 0.83% (95% CI, 0.76%-0.91%) in those without atrial fibrillation. At 1 year after noncardiac surgery, cumulative rates of stroke were 1.47% (95% CI, 1.24%-1.75%) in those with perioperative atrial fibrillation and 0.36% (95% CI, 0.35%-0.37%) in those without atrial fibrillation. In a Cox proportional hazards analysis accounting for potential confounders, perioperative atrial fibrillation was associated with subsequent stroke both after cardiac surgery (hazard ratio, 1.3; 95% CI, 1.1-1.6) and noncardiac surgery (hazard ratio, 2.0; 95% CI, 1.7-2.3). The association was significantly stronger for perioperative atrial fibrillation after noncardiac vs cardiac surgery (P less than .001 for interaction).
We have no way of knowing the duration of a fib in these patients but, likely, many episodes were transient.
Friday, November 28, 2014
Perioperative beta blockers: an update
The pendulum regarding perioperative beta blockers has been swinging. Nevertheless, evidence accumulated during this time offers reasonable guidance for clinicians. Via CCJM.
Surgery in patients taking new (target specific) oral anticoagulants
From a recent review in CCJM:
The article summarizes the current thinking. It gives a nice summary of the pharmacokinetics and pharmacodynamics, and practical information for the perioperative period. A guide for timing of discontinuation of TSOACs prior to surgery is found in this table.
While various periprocedural protocols for TSOAC therapy have been proposed, evidence-based guidelines are still to come.
The article summarizes the current thinking. It gives a nice summary of the pharmacokinetics and pharmacodynamics, and practical information for the perioperative period. A guide for timing of discontinuation of TSOACs prior to surgery is found in this table.
Thursday, November 27, 2014
The risk of GI bleeding associated with SSRIs with and without NSAIDs
Here are the findings of a recent systematic review and meta-analysis:
RESULTS: Fifteen case–control studies (including 393,268 participants) and four cohort studies were included in the analysis. There was an increased risk of upper GI bleeding with SSRI medications in the case–control studies (OR=1.66, 95% CI=1.44,1.92) and cohort studies (OR=1.68, 95% CI=1.13,2.50). The number needed to harm for upper GI bleeding with SSRI treatment in a low-risk population was 3,177, and in a high-risk population it was 881. The risk of upper GI bleeding was further increased with the use of both SSRI and NSAID medications (OR=4.25, 95% CI=2.82,6.42).
CONCLUSIONS: SSRI medications are associated with a modest increase in the risk of upper GI bleeding, which is lower than has previously been estimated. This risk is significantly elevated when SSRI medications are used in combination with NSAIDs, and physicians prescribing these medications together should exercise caution and discuss this risk with patients.
Wednesday, November 26, 2014
More evidence that dabigatran increases the risk of MI
From a recent meta-analysis:
Background Signals of an increased risk of myocardial infarction (MI) have been identified with dabigatran etexilate in randomized controlled trials (RCTs).
Methods and Resules We conducted searches of the published literature and a clinical trials registry maintained by the drug manufacturer. Criteria for inclusion in our meta‐analysis included all RCTs and the availability of outcome data for MI, other cardiovascular events, major bleeding, and all‐cause mortality. Among the 501 unique references identified, 14 RCTs fulfilled the inclusion criteria. Stratification analyses by comparators and doses of dabigatran etexilate were conducted. Peto odds ratio (ORPETO) values using the fixed‐effect model (FEM) for MI, other cardiovascular events, major bleeding, and all‐cause mortality were 1.34 (95% CI 1.08 to 1.65, P=0.007), 0.93 (95%CI 0.83 to 1.06, P=0.270), 0.88 (95% CI 0.79 to 0.99, P=0.029), and 0.89 (95% CI 0.80 to 1.00, P=0.041). When compared with warfarin, ORPETO values using FEM were 1.41 (95% CI 1.11 to 1.80, P=0.005), 0.94 (95%CI 0.83 to 1.06, P=0.293), 0.85 (95% CI 0.76 to 0.96, P=0.007), and 0.90 (95% CI 0.81 to 1.01, P=0.061), respectively. In RCTs using the 150‐mg BID dosage, the ORPETO values using FEM were 1.45 (95% CI 1.11 to 1.91, P=0.007), 0.95 (95% CI 0.82 to 1.09, P=0.423), 0.92 (95% CI 0.81 to 1.05, P=0.228), and 0.88 (95% CI 0.78 to 1.00, P=0.045), respectively. The results of the 110‐mg BID dosage were mainly driven by the RE‐LY trial.
Conclusions This meta‐analysis provides evidence that dabigatran etexilate is associated with a significantly increased risk of MI. This increased risk should be considered taking into account the overall benefit in terms of major bleeding and all‐cause mortality.
The data analysis is complex and it is helpful to read the body of the paper (free full test), particularly Table 2, for clarity.
Tuesday, November 25, 2014
Monday, November 24, 2014
Heart failure performance and outcomes
Here's a recent paper in JACC with some interesting findings:
I interject here to point out this important distinction. If the primary diagnosis is heart failure the hospital is under the “report card” and financial incentive of the heart failure performance measures. If the heart failure patient is discharged under a different primary diagnosis (with heart failure as a secondary) the hospital is not under the incentive. Keep that in mind in reading the results:
So if heart failure is the principal diagnosis and the performance game is in play, participants adhere at a higher rate. That isn't surprising. What surprised me is that the differences were not greater. More interesting to me, though, was the improvement in outcomes associated with following the measures. On the one hand the finding is intuitive; after all, the administration of neurohumeral antagonists guided by assessment of ventricular function is evidence based and would be expected to help patients. On the other hand it is a new finding, in disagreement with prior research, which failed to show that such inherently beneficial and evidence based therapies made a difference in outcomes when associated with performance incentives.
As expressed many times here on the blog, I have a contrarian view of performance measures. This study doesn't change that view much. ACEIs and ARBs seemed to help patients whether their prescription was performance driven or not. The performance driven population (those with a primary diagnosis of heart failure) reflected slightly higher utilization than the comparison group and one could therefore infer that the incentive drove a modest reduction in mortality. Moreover, the idea is plausible. However, as cited in an accompanying editorial, the finding is in contrast to the prior body of research, not only for heart failure but across the whole range of performance measures.
Therein lies the conundrum: take an evidence based treatment (one proven in clinical trials to be beneficial), put it in a public incentive package and it no longer seems to work. The reason is that the way performance is structured, providers are incented to game the system mainly through coding and charting. That, they have discovered, is where the low hanging fruit is for reimbursement and favorable public reporting. Thus performance is not a valid surrogate for quality, either as a driver of patient care or a way to measure it.
Methods We assessed rates of compliance with care measures for patients hospitalized with acute or chronic heart failure in the ARIC (Atherosclerosis Risk In Communities) study surveillance catchment area from 2005 to 2009. Rates of compliance were compared between patients with a principal discharge diagnosis of heart failure and those with another principal discharge diagnosis.
I interject here to point out this important distinction. If the primary diagnosis is heart failure the hospital is under the “report card” and financial incentive of the heart failure performance measures. If the heart failure patient is discharged under a different primary diagnosis (with heart failure as a secondary) the hospital is not under the incentive. Keep that in mind in reading the results:
Results Of 4,345 hospitalizations of heart failure patients, 39.6% carried a principal diagnosis of heart failure. Patients with a principal heart failure diagnosis had higher rates of LV function assessment (89.1% vs. 82.5%; adjusted prevalence ratio [aPR]: 1.07; 95% confidence interval [CI]: 1.04 to 1.10) and discharge ACE inhibitor/angiotensin receptor blocker (ARB) in LV dysfunction (64.1% vs. 56.3%; aPR: 1.11; 95% CI: 1.03 to 1.20) as compared to patients hospitalized for another cause. LV assessment and ACE inhibitor/ARB use were associated with reductions in 1-year post-discharge mortality (adjusted odds ratio: 0.66, 95% CI: 0.51 to 0.85; adjusted odds ratio: 0.72, 95% CI: 0.54 to 0.96, respectively) that did not differ for patients with versus without a principal heart failure diagnosis.
So if heart failure is the principal diagnosis and the performance game is in play, participants adhere at a higher rate. That isn't surprising. What surprised me is that the differences were not greater. More interesting to me, though, was the improvement in outcomes associated with following the measures. On the one hand the finding is intuitive; after all, the administration of neurohumeral antagonists guided by assessment of ventricular function is evidence based and would be expected to help patients. On the other hand it is a new finding, in disagreement with prior research, which failed to show that such inherently beneficial and evidence based therapies made a difference in outcomes when associated with performance incentives.
As expressed many times here on the blog, I have a contrarian view of performance measures. This study doesn't change that view much. ACEIs and ARBs seemed to help patients whether their prescription was performance driven or not. The performance driven population (those with a primary diagnosis of heart failure) reflected slightly higher utilization than the comparison group and one could therefore infer that the incentive drove a modest reduction in mortality. Moreover, the idea is plausible. However, as cited in an accompanying editorial, the finding is in contrast to the prior body of research, not only for heart failure but across the whole range of performance measures.
Therein lies the conundrum: take an evidence based treatment (one proven in clinical trials to be beneficial), put it in a public incentive package and it no longer seems to work. The reason is that the way performance is structured, providers are incented to game the system mainly through coding and charting. That, they have discovered, is where the low hanging fruit is for reimbursement and favorable public reporting. Thus performance is not a valid surrogate for quality, either as a driver of patient care or a way to measure it.
Sunday, November 23, 2014
A process improvement tool for acute pancreatitis
From a recent article in the American Journal of Gastroenterology:
METHODS: Design/Setting: Observational study, entitled, The AP Early Response (TAPER) Project. Tertiary center emergency department (ED) and hospital. Participants: Two consecutive samplings of patients having ICD-9 code (577.0) for AP were generated from the emergency department (ED) or hospital admissions. Diagnosis of AP was based on conventional Atlanta criteria. The Pre-TAPER-CDS-Tool group (5/30/06–6/22/07) had 110 patients presenting to the ED with AP per 976 ICD-9 (577.0) codes and the Post-TAPER-CDS-Tool group (5/30/06–6/22/07) had 113 per 907 ICD-9 codes (7/14/10–5/5/11).
Intervention: The TAPER-CDS-Tool, developed 12/2008–7/14/2010, is a combined early, automated paging-alert system, which text pages ED clinicians about a patient with AP and an intuitive web-based point-of-care instrument, consisting of seven early management recommendations.
RESULTS: The pre- vs. post-TAPER-CDS-Tool groups had similar baseline characteristics. The post-TAPER-CDS-Tool group met two management goals more frequently than the pre-TAPER-CDS-Tool group: risk stratification (P less than 0.0001) and intravenous fluids greater than 6L/1st 0–24 h (P=0.0003). Mean (s.d.) hospital LOS was significantly shorter in the post-TAPER-CDS-Tool group (4.6 (3.1) vs. 6.7 (7.0) days, P=0.0126). Multivariate analysis identified four independent variables for hospital LOS: the TAPER-CDS-Tool associated with shorter LOS (P=0.0049) and three variables associated with longer LOS: Japanese severity score (P=0.0361), persistent organ failure (P=0.0088), and local pancreatic complications (less than 0.0001).
CONCLUSIONS: The TAPER-CDS-Tool is associated with changed clinician behavior and shortened hospital LOS, which has significant financial implications.
Saturday, November 22, 2014
Methamphetamine cardiomyopathy (MAC)
Here are some key points from a review:
MAC is a newly emerging entity and is somewhat poorly understood.
It appears to be mainly a dilated cardiomyopathy (systolic dysfunction).
It appears to be reversible upon cessation of the ingestion, acknowledging that there may be a point in time of irreversibility.
It is believed to be catecholamine mediated and as such has features in common with stress cardiomyopathy, including pathologic findings of contraction band necrosis.
MAC is a newly emerging entity and is somewhat poorly understood.
It appears to be mainly a dilated cardiomyopathy (systolic dysfunction).
It appears to be reversible upon cessation of the ingestion, acknowledging that there may be a point in time of irreversibility.
It is believed to be catecholamine mediated and as such has features in common with stress cardiomyopathy, including pathologic findings of contraction band necrosis.
Friday, November 21, 2014
Should patient satisfaction ever be 100%?
That could be dangerous! Great post and fascinating comment thread over at The Happy MD.
Procalcitonin guided therapy in critically ill patients
Shorter lengths of stay, shorter durations of antibiotic therapy at no cost in terms of outcome, in this study.
Thursday, November 20, 2014
Severity assessment in pulmonary embolism: a need for consistency
As it does for many conditions, severity assessment of pulmonary embolism guides treatment. Severity assessment for PE is more important than ever these days because treatment options have multiplied. There are now many more decision points than we had just a few years ago. Now under discussion, for example, is the question of which patients can be discharged early or even undergo the entirety of their treatment as outpatients. The approval of target specific oral anticoagulants adds another decision point. Which patients with PE are candidates for those agents? Recent discussions have asked the question of whether there exists a subset of patients with acute PE who don't need to be treated at all. A clinical trial now in progress seeks to address that question. The question regarding how long to anticoagulate patients for secondary prevention is not as open and shut as it was just a few years ago. This is illustrated by a reading of the most recent ACCP guidelines. The same is true regarding indications for IVC filters. Meanwhile the debate about selection of patients for thrombolytic therapy rages on and has recently been complicated by promising studies looking at half dose thrombolytic therapy for a variety of patients with pulmonary embolism.
For us to make sense of all the new evidence and treatment options severity classification becomes important. The problem is this area is evolving too and has become inconsistent across the published literature. I'm going to be blogging about some of the new treatment options in the near future. But in order to have a meaningful discussion it is first important to define the terms of severity classification. What follows is my attempt to review some of the history of PE classification and outline the topic as it stands now, however confusing.
Back in the day it was pretty simple. The binary decision was whether to treat conventionally (with unfractionated or low molecular weight heparin) or to use thrombolytic therapy. It was based on whether the PE was associated with normal blood pressure or hypotension respectively. PE with hypotension correlated with obliteration of 50% or more of the activity on radionuclide perfusion scanning, which was an ancillary criterion. There followed a rising awareness of patients who were normotensive but had a large clot burden and evidence of acute right ventricular dysfunction as measured by biomarkers and/or imaging which consisted usually of echocardiograhy as well, in some centers, as ascertainment of the ratio of right ventricular to left ventricular diameter on CT angiography. With the addition of this intermediate category we then had 3 categories which became known as massive, submassive and hemodynamically normal.
Treatment discussions regarding pulmonary embolism have centered around this classification. For massive PE there has been a fairly strong consensus in favor of thrombolytic therapy in the absence of contraindications. Submassive PEs are the subject of controversy with divided opinion on whether to treat with thrombolysis or conventional heparin therapy with the weight of opinion favoring the latter. Hemodynamically uncomplicated PEs according to the recent thinking are those that could be treated with conventional anticoagulation and considered for early discharge or even outpatient treatment.
With the publication of recent papers suggesting yet another treatment method, half dose thrombolytic in conjunction with anticoagulation, the discussion has been complicated further because these papers have used yet another classification, which stratifies pulmonary emboli into severe, moderate and (by implication) mild forms. The problem is, this new classification does not translate well into the traditional one because it uses criteria (mainly anatomic) that are not analogous. This is illustrated by the MOPETT trial and the more recent drip, dose and discharge (DDD) paper. Here are the definitions form the DDD paper:
MOPETT did not define severe PE because those patients were not studied. The definition of moderate PE was along the same lines as in DDD with a slight variation:
In order to have a meaningful discussion of the rapidly emerging literature and treatment options for pulmonary embolism it is important to keep these definitions in mind. In the future we need some sort of a consensus.
For us to make sense of all the new evidence and treatment options severity classification becomes important. The problem is this area is evolving too and has become inconsistent across the published literature. I'm going to be blogging about some of the new treatment options in the near future. But in order to have a meaningful discussion it is first important to define the terms of severity classification. What follows is my attempt to review some of the history of PE classification and outline the topic as it stands now, however confusing.
Back in the day it was pretty simple. The binary decision was whether to treat conventionally (with unfractionated or low molecular weight heparin) or to use thrombolytic therapy. It was based on whether the PE was associated with normal blood pressure or hypotension respectively. PE with hypotension correlated with obliteration of 50% or more of the activity on radionuclide perfusion scanning, which was an ancillary criterion. There followed a rising awareness of patients who were normotensive but had a large clot burden and evidence of acute right ventricular dysfunction as measured by biomarkers and/or imaging which consisted usually of echocardiograhy as well, in some centers, as ascertainment of the ratio of right ventricular to left ventricular diameter on CT angiography. With the addition of this intermediate category we then had 3 categories which became known as massive, submassive and hemodynamically normal.
Treatment discussions regarding pulmonary embolism have centered around this classification. For massive PE there has been a fairly strong consensus in favor of thrombolytic therapy in the absence of contraindications. Submassive PEs are the subject of controversy with divided opinion on whether to treat with thrombolysis or conventional heparin therapy with the weight of opinion favoring the latter. Hemodynamically uncomplicated PEs according to the recent thinking are those that could be treated with conventional anticoagulation and considered for early discharge or even outpatient treatment.
With the publication of recent papers suggesting yet another treatment method, half dose thrombolytic in conjunction with anticoagulation, the discussion has been complicated further because these papers have used yet another classification, which stratifies pulmonary emboli into severe, moderate and (by implication) mild forms. The problem is, this new classification does not translate well into the traditional one because it uses criteria (mainly anatomic) that are not analogous. This is illustrated by the MOPETT trial and the more recent drip, dose and discharge (DDD) paper. Here are the definitions form the DDD paper:
Moderate PE was regarded as presence of symptoms plus objective evidence of PE, defined as 70% involvement of a pulmonary artery or 2 lobar or 4 segmental branches plus hemodynamic stability. Severe PE was defined as systolic blood pressure less than of equal to100 mm Hg plus all other features of moderate PE; saddle pulmonary embolism; or involvement of greater than 70% of the main pulmonary artery (PA) with thrombus, irrespective of blood pressure.
MOPETT did not define severe PE because those patients were not studied. The definition of moderate PE was along the same lines as in DDD with a slight variation:
“Moderate” PE was defined as the presence of signs and symptoms of PE plus computed tomographic pulmonary angiographic involvement of greater than 70% involvement of thrombus in greater than or equal to 2 lobar of left or right main pulmonary arteries or by a high probability ventillation/perfusion scan showing ventillation/perfusion mismatch in greater than or equal to two lobes.
In order to have a meaningful discussion of the rapidly emerging literature and treatment options for pulmonary embolism it is important to keep these definitions in mind. In the future we need some sort of a consensus.
Neuraminidase inhibitors for influenza: what does the evidence really show?
This has been the subject of controversy. Here is an evidence summary published in a recent issue of the Annals of Energency Medicine. From the article:
So we have high level data in support of NI based on soft outcomes (time to symptom relief) and low level data in support of them for hard outcomes (severe complications, death). The debate about this has been heated and overhyped. The final answer is that it depends on your evidence quality threshold, your preferences and your values.
This Cochrane review demonstrates that oseltamivir shortens symptom duration by 21 hours in patients who receive the drug within 48 hours of symptom onset. Unfortunately, there is little information that can be inferred from current available data about hospitalization rates and neuraminidase inhibitors’ effectiveness in decreasing transmission rates of the influenza virus. However, the CDC continues to recommend neuraminidase inhibitors, using information based on observational studies that showed decreased hospital stays and severe outcomes such as ICU admissions or death in patients treated with oseltamivir.3
In the past, Cochrane reviews examining the effect of neuraminidase inhibitors were based on published clinical studies conducted by drug manufacturers; however, these studies were found to reflect only a small portion of the trials conducted and bore discrepancies with their clinical study report counterparts. For the first time in Cochrane history, this review attempted to remove the reporting bias seen in the previous reviews by analyzing the unpublished regulatory data from clinical study reports rather than relying on the published trials.4 Unfortunately, despite major efforts by the systematic review authors, they were unable to obtain much of the data from trials sponsored by the drug manufacturers.
So we have high level data in support of NI based on soft outcomes (time to symptom relief) and low level data in support of them for hard outcomes (severe complications, death). The debate about this has been heated and overhyped. The final answer is that it depends on your evidence quality threshold, your preferences and your values.
Performance and quality: more evidence of non evidence
From JAMA Internal Medicine:
Related commentary from ACP Hospitalist Weekly:
Unwise indeed. Moreover, guidelines for VTE prophylaxis in medical patients are sufficiently restrictive that it is unlikely that 95% of patients would be candidates. Performance driven initiatives tend to push the number higher than appropriate, however.
Importance Hospitalization for acute medical illness is associated with increased risk of venous thromboembolism (VTE). Although efforts designed to increase use of pharmacologic VTE prophylaxis are intended to reduce hospital-associated VTE, whether higher rates of prophylaxis reduce VTE in medical patients is unknown.
Objective To examine the association between pharmacologic VTE prophylaxis rates and hospital-associated VTE.
Design, Setting, and Participants Retrospective, multicenter cohort study conducted at 35 Michigan hospitals participating in a statewide quality collaborative from January 1, 2011, through September 13, 2012. Trained medical record abstractors at each hospital collected data from 31 260 general medical patients. Use of VTE prophylaxis on admission, VTE risk factors, and VTE events 90 days after hospital admission were recorded using a combination of medical record review and telephone follow-up. Hospitals were grouped into tertiles of performance based on rate of pharmacologic prophylaxis use on admission for at-risk patients.
Main Outcomes and Measures Association between hospital performance and time to development of VTE within 90 days of hospital admission.
Results A total of 14 563 of 20 794 patients (70.0%) eligible for pharmacologic prophylaxis received prophylaxis on admission. The rates of pharmacologic prophylaxis use at hospitals in the high-, moderate-, and low-performance tertiles were 85.8%, 72.6%, and 55.5%, respectively. A total of 226 VTE events occurred during 1 765 449 days of patient follow-up. Compared with patients at hospitals in the highest-performance tertile, the hazard of VTE in patients at hospitals in moderate-performance (hazard ratio, 1.10; 95% CI, 0.74-1.62) and low-performance (hazard ratio, 0.96, 95% CI, 0.63-1.45) tertiles did not differ after adjusting for potential confounders. Results remained robust when examining mechanical prophylaxis, prophylaxis use throughout the hospitalization, and subsequent inpatient stays after discharge from the index hospitalization.
Conclusions and Relevance The occurrence of 90-day VTE in medical patients after hospitalization is low. Patients who receive care at hospitals that have lower rates of pharmacologic prophylaxis do not have higher adjusted hazards of VTE, even after accounting for individual receipt of pharmacologic prophylaxis.
Related commentary from ACP Hospitalist Weekly:
The findings suggest that "efforts to broadly increase rates of pharmacologic prophylaxis in non-critically ill general medical patients may not yield significant reductions in hospital-associated (VTE)," the authors wrote. Some of the past studies that found an association between using prophylaxis and lower VTE rates included patients with higher baseline risk of VTE like surgical patients, and patients with longer average lengths of stay than the typical medical service patient, they wrote. Many VTE experts and toolkits support an approach that would result in up to 95% of inpatients receiving prophylaxis, but "our study questions the wisdom of that approach," they wrote.
Unwise indeed. Moreover, guidelines for VTE prophylaxis in medical patients are sufficiently restrictive that it is unlikely that 95% of patients would be candidates. Performance driven initiatives tend to push the number higher than appropriate, however.
Wednesday, November 19, 2014
Gruber and stupid voters
Via FIRM. I wonder how many other policy makers feel that way and just didn't get caught. I wonder, too, how many of them feel that way about practicing physicians.
Choice of resuscitation crystalloid and mortality in sepsis
From a recent study:
Design: A retrospective cohort study of patients admitted with sepsis, not undergoing any surgical procedures, and treated in an ICU by hospital day 2. We used propensity score matching to control for confounding and compared the following outcomes after resuscitation with balanced versus with no-balanced fluids: in-hospital mortality, acute renal failure with and without dialysis, and hospital and ICU lengths of stay. We also estimated the dose-response relationship between receipt of increasing proportions of balanced fluids and in-hospital mortality.
Setting: Three hundred sixty U.S. hospitals that were members of the Premier Healthcare alliance between November 2005 and December 2010.
Patients: A total of 53,448 patients with sepsis, treated with vasopressors and crystalloids in an ICU by hospital day 2 including 3,396 (6.4%) that received balanced fluids.
Interventions: None.
Measurements and Main Results: Patients treated with balanced fluids were younger and less likely to have heart or chronic renal failure, but they were more likely to receive mechanical ventilation, invasive monitoring, colloids, steroids, and larger crystalloid volumes (median 7 vs 5 L). Among 6,730 patients in a propensity-matched cohort, receipt of balanced fluids was associated with lower in-hospital mortality (19.6% vs 22.8%; relative risk, 0.86; 95% CI, 0.78, 0.94). Mortality was progressively lower among patients receiving larger proportions of balanced fluids. There were no significant differences in the prevalence of acute renal failure (with and without dialysis) or in-hospital and ICU lengths of stay.
Conclusions: Among critically ill adults with sepsis, resuscitation with balanced fluids was associated with a lower risk of in-hospital mortality. If confirmed in randomized trials, this finding could have significant public health implications, as crystalloid resuscitation is nearly universal in sepsis.
A recent systematic review of health information technology
This updated systematic review on the effects of HIT recently appeared in the Annals of Internal Medicine. The focus was on meaningful use aspects, particularly clinical decision support and CPOE. A few studies looked at the effect of patients' access to their own EMRs. The results were mixed but tended to be positive. The vast majority of reports were on processes or very low level surrogates, with very few studies looking at meaningful clinical outcomes. Among those, however, were a couple of reports suggesting reduced mortality attributable to HIT.
Patient engagement in hospital medicine
A recent post on patient engagement for hospitalists offers these suggestions:
Those are great ideas although I have a problem with item 2. Few patients, even among the most intelligent lay persons, have the ability to interpret raw clinical data in a way that is useful for medical decision making.
Patient engagement is not a new idea. In fact, it's old school (I mean that in a good way). It was one of the key tenets of evidence based medicine, a movement launched in 1992. Because of its focus on the individual patient it does not work well with top-down, pathway driven or population based medicine.
The biggest barrier to this type of medicine is a lack of time as I pointed out before. [1] [2] Unintentionally, and to its potential embarrassment, the medical profession has increasingly attempted to circumvent the time problem by involving the discipline of palliative care as I once explained:
Palliative care is nothing more than good primary care. Or what an excellent internist or hospitalist should be doing. So yes, there is a definition for palliative care but it goes unspoken because the profession is, or should be, embarrassed by the fact that we need a “specialty” whose focus is to offload the rest of us from doing all those things that make for excellence in comprehensive care because we don't have the time.
1. Encouraging patients to ask questions when they see their doctor every day
As simple as it sounds, this is not done nearly enough, and is a big missed opportunity to make a difference to patients’ understanding of their illness...
2. Giving patients all the knowledge they need about their medical condition
Writing details such as blood count numbers on the whiteboard at the end of their bed is one way to do this. In the future, patients will likely be able to pull up some of their own data on computers. The more that patients know, the more empowered they will be to make important health care decisions.
3. Involvement of families
Just as important as the patient, is the family. This is true for any patient who is too unwell to speak for themselves, and particularly applies to the elderly...
4. Involving the patient fully in the discharge process
The discharge process by its’ very nature is a risky endeavor. Typically there are medications that have been changed, tests pending, or even an uncertain diagnosis. All this at a time when the patient is still very frail. It is a crucial transition point, more important than almost any other to get right.
5. Follow-up care
All hospitalized patients must follow-up in a timely manner after being discharged. Nipping a potential problem in the bud can help reduce readmissions and potentially serious complications.
Those are great ideas although I have a problem with item 2. Few patients, even among the most intelligent lay persons, have the ability to interpret raw clinical data in a way that is useful for medical decision making.
Patient engagement is not a new idea. In fact, it's old school (I mean that in a good way). It was one of the key tenets of evidence based medicine, a movement launched in 1992. Because of its focus on the individual patient it does not work well with top-down, pathway driven or population based medicine.
The biggest barrier to this type of medicine is a lack of time as I pointed out before. [1] [2] Unintentionally, and to its potential embarrassment, the medical profession has increasingly attempted to circumvent the time problem by involving the discipline of palliative care as I once explained:
Palliative care is nothing more than good primary care. Or what an excellent internist or hospitalist should be doing. So yes, there is a definition for palliative care but it goes unspoken because the profession is, or should be, embarrassed by the fact that we need a “specialty” whose focus is to offload the rest of us from doing all those things that make for excellence in comprehensive care because we don't have the time.
Tuesday, November 18, 2014
Cholesterol efflux capacity correlates inversely with incident cardiovascular events
Study results were announced at AHA and published in NEJM.
IMPROVE-IT results announced
Here are the results presented at the AHA meetings as reported by Cardiobrief:
The NNT of 50, when spread out over 6 years, is not huge. This represents a modest incremental benefit which is the best we would have reasonably hoped for given that the patients were already on statins and their baseline LDL levels were low.
The real impact of this study, in my view, is on the debate over whether LDL lowering matters. Findings about the pleiotropic effects of statins in recent years somehow led to the notion that LDL reduction was irrelevant. That simplistic thinking took hold despite lots of prior evidence that LDL reduction reduced cardiovascular events no matter by what means. Some even spun the new lipid guidelines as a debunking of the LDL hypothesis. IMPROVE-IT adds further support to LDL reduction.
The Improved Reduction of Outcomes: Vytorin Efficacy International Trial, presented Monday morning at the American Heart Association meeting in Chicago, randomized 18,144 high-risk patients within 10 days of an acute coronary event to either ezetimibe or placebo on top of a statin. These patients had LDL levels between 50-125 mg/dL, or between 50-100 mg/dL if on a prior cholesterol drug. Patients were followed for an average of six years. The trial ended after there were 5,250 primary endpoint events (CV death, MI, hospital admission for unstable angina, coronary revascularization more than a month after randomization, or stroke).
Primary endpoint events occurred in 34.7% of the control group versus 32.7% of the treatment group, representing a 6.4% reduction in risk (HR 0.936, CI 0.887-0.988, p=0.016). The investigators calculated that 50 patients would need to be treated for seven years to prevent one event.
The NNT of 50, when spread out over 6 years, is not huge. This represents a modest incremental benefit which is the best we would have reasonably hoped for given that the patients were already on statins and their baseline LDL levels were low.
The real impact of this study, in my view, is on the debate over whether LDL lowering matters. Findings about the pleiotropic effects of statins in recent years somehow led to the notion that LDL reduction was irrelevant. That simplistic thinking took hold despite lots of prior evidence that LDL reduction reduced cardiovascular events no matter by what means. Some even spun the new lipid guidelines as a debunking of the LDL hypothesis. IMPROVE-IT adds further support to LDL reduction.
Antibiotics for severe sepsis and septic shock: the earlier the better
Here are results from the Surviving Sepsis Campaign database confirming what we already knew.
Recruitment maneuvers in ARDS: systematic review and meta-analysis
From a recent paper:
Results
Our database search identified ten RCTs (1,594 patients, 612 events) which satisfied the inclusion criteria. The meta-analysis assessing the effect of ARMs on in-hospital mortality showed a risk ratio (RR) of 0.84 [95 % confidence interval (CI) 0.74–0.95; I2 = 0 %], although the quality of evidence was considered to be low due to the risk of bias in the included trials and the indirectness of the evidence—that is, ARMs were usually conducted together with other ventilatory interventions which may affect the outcome of interest. There were no differences in the rates of barotrauma (RR 1.11; 95 % CI 0.78–1.57; I2 = 0 %) or need for rescue therapies (RR 0.76, 95 % CI 0.41–1.40; I2 = 56 %). Most trials found no difference between groups in terms of duration of mechanical ventilation and length of stay in the intensive care unit and hospital. The TSA showed that the available evidence for the effect of ARMs on in-hospital mortality is precise in the case of a type I error of 5 %, but it is not precise with a type I error of 1 %.
Conclusions
Although ARMs may decrease the mortality of patients with ARDS without increasing the risk for major adverse events, current evidence is not definitive. Large-scale ongoing trials addressing this question may provide data better applicable to clinical practice.
If an ICD is not proven beneficial early post MI why bridge with a life vest?
An interesting discussion at Cardiobrief.
Monday, November 17, 2014
Post marketing controversy over dabigatran
Questions have been swirling around the use of dabigatran in light of some recent post marketing data. These concerns were recently hyped by the blogger at Emergency Medicine Literature of Note in a post titled No Good Ever Comes of Dabigatran.
It revolves around two recently published papers on the post marketing experience. The news is not all bad.
First from JAMA Internal Medicine:
Then this from Circulation:
There's nothing shocking here that I can see. It appears that any excess bleeding attributable to dabigatran was driven by GI events, which we already knew from RE-LY. We also knew that the performance of most new drugs is better in clinical trials than in the real world.
As more post marketing experience comes in this story will continue to unfold for dabigatran and the other newly approved anticoagulants. There are no pat answers available at this point.
More from ACP Hospitalist Weekly.
It revolves around two recently published papers on the post marketing experience. The news is not all bad.
First from JAMA Internal Medicine:
Importance It remains unclear whether dabigatran etexilate mesylate is associated with higher risk of bleeding than warfarin sodium in real-world clinical practice.
Objective To compare the risk of bleeding associated with dabigatran and warfarin using Medicare data.
Design, Setting, and Participants In this retrospective cohort study, we used pharmacy and medical claims in 2010 to 2011 from a 5% random sample of Medicare beneficiaries. We identified participants as those newly diagnosed as having atrial fibrillation from October 1, 2010, through October 31, 2011, and who initiated dabigatran or warfarin treatment within 60 days of initial diagnosis. We followed up patients until discontinued use or switch of anticoagulants, death, or December 31, 2011.
Exposures Dabigatran users (n = 1302) and warfarin users (n = 8102)...
Results Dabigatran was associated with a higher risk of bleeding relative to warfarin, with hazard ratios of 1.30 (95% CI, 1.20-1.41) for any bleeding event, 1.58 (95% CI, 1.36-1.83) for major bleeding, and 1.85 (95% CI, 1.64-2.07) for gastrointestinal bleeding. The risk of intracranial hemorrhage was higher among warfarin users, with a hazard ratio of 0.32 (95% CI, 0.20-0.50) for dabigatran compared with warfarin. Dabigatran was consistently associated with an increased risk of major bleeding and gastrointestinal hemorrhage for all subgroups analyzed. The risk of major bleeding among dabigatran users was especially high for African Americans and patients with chronic kidney disease.
Conclusions and Relevance Dabigatran was associated with a higher incidence of major bleeding (regardless of the anatomical site), a higher risk of gastrointestinal bleeding, but a lower risk of intracranial hemorrhage. Thus, dabigatran should be prescribed with caution, especially among high-risk patients.
Then this from Circulation:
Methods and Results—We formed new-user cohorts of propensity score matched elderly patients enrolled in Medicare, who initiated dabigatran or warfarin for treatment of non-valvular AF between October 2010 and December 2012. Among 134,414 patients with 37,587 person-years of follow-up, there were 2,715 primary outcome events. The hazard ratios (95% confidence intervals) comparing dabigatran with warfarin (reference) were ischemic stroke: 0.80 (0.67-0.96); intracranial hemorrhage: 0.34 (0.26-0.46); major gastrointestinal bleeding: 1.28 (1.14-1.44); acute myocardial infarction: 0.92 (0.78-1.08); and death: 0.86 (0.77-0.96). In the subgroup treated with dabigatran 75 mg twice daily, there was no difference in risk compared with warfarin for any outcome except intracranial hemorrhage, where dabigatran risk was reduced. Most patients treated with dabigatran 75 mg twice daily appeared not to have severe renal impairment, the intended population for this dose. In the dabigatran 150 mg twice daily subgroup, the magnitude of effect for each outcome was greater than in the combined-dose analysis.
Conclusions—In general practice settings, dabigatran was associated with reduced risk of ischemic stroke, intracranial hemorrhage, and death, and increased risk of major gastrointestinal hemorrhage compared with warfarin in elderly patients with non-valvular AF. These associations were most pronounced in patients treated with dabigatran 150 mg twice daily, whereas the association of 75 mg twice daily with study outcomes was indistinguishable from warfarin except for a lower risk of intracranial hemorrhage with dabigatran.
There's nothing shocking here that I can see. It appears that any excess bleeding attributable to dabigatran was driven by GI events, which we already knew from RE-LY. We also knew that the performance of most new drugs is better in clinical trials than in the real world.
As more post marketing experience comes in this story will continue to unfold for dabigatran and the other newly approved anticoagulants. There are no pat answers available at this point.
More from ACP Hospitalist Weekly.
Patient safety: where have we gone wrong?
It is pretty widely accepted that the patient safety movement has been a failure. The authors of this paper in the Annals of Internal Medicine cite a lot of reasons and conclude:
Good evidence exists that educating caregivers about safety science and improving safety culture is the foundation of improvement efforts. Of course, reliance on the line worker is a long-standing tenet of quality improvement across many industries. With the emerging evidence that safety is not improving and is too heterogeneous to be assessed by externally mandated measures, we conclude that external top-down efforts to measure safety should cease to expand. We should measure what matters by focusing on creating a positive safety culture, developing HIT tools to detect local safety problems, and training frontline caregivers to improve patient safety.
Pain management dogma and the opiate prescription epidemic
A recent post at Academic Life in Emergency Medicine talked about an epidemic of opiate prescriptions and the associated spike in mortality. The post and a related article in the Annals of Emergency Medicine focused primarily on the concerns of emergency medicine providers but it has more general applicability.
The article deals with multiple dimensions of the problem including the need for educational and even regulatory guidance. One point that particularly interested me has been the focus of many of my older posts this topic over the years which is that this epidemic got started with the “pain the fifth vital sign” initiative that began about a decade and a half ago. It's hardly coincidental that the opiate related fatalities started rising in 1999. The Institute of Medicine, the pharmaceutical industry and our own professional societies were among the many accomplices.
The “educational” piece of the campaign obfuscated the medical lexicon and elevated dogma over science. Worse, it was illogical. How, for example, could something so culturally driven and subjective as the symptom of pain be a vital sign? Nevertheless the campaign was so powerfully leveraged that administrators and physicians were wowed and cowed. Finally some are taking a more critical view of things. I recently posted this retrospective on some of the original tenets of the movement. A decade ago no one dared challenge them. Looking back now it would be humorous had the effects not been so devastating. From that post:
It's great to see that some people are finally saying enough is enough.
The article deals with multiple dimensions of the problem including the need for educational and even regulatory guidance. One point that particularly interested me has been the focus of many of my older posts this topic over the years which is that this epidemic got started with the “pain the fifth vital sign” initiative that began about a decade and a half ago. It's hardly coincidental that the opiate related fatalities started rising in 1999. The Institute of Medicine, the pharmaceutical industry and our own professional societies were among the many accomplices.
The “educational” piece of the campaign obfuscated the medical lexicon and elevated dogma over science. Worse, it was illogical. How, for example, could something so culturally driven and subjective as the symptom of pain be a vital sign? Nevertheless the campaign was so powerfully leveraged that administrators and physicians were wowed and cowed. Finally some are taking a more critical view of things. I recently posted this retrospective on some of the original tenets of the movement. A decade ago no one dared challenge them. Looking back now it would be humorous had the effects not been so devastating. From that post:
What still baffles me is why so many doctors accepted the biggest and most obvious load of nonsense, the idea that pain, long established in clinical medicine as a symptom, could suddenly become a sign. Even The Joint Commission and my own professional organization, the Society of Hospital Medicine (then known as NAIP) were serving the Kool-aid.
Other nutty ideas were promulgated:
Opiates are safe.
Uh huh. How's that working these days?
Doctors' concerns about opiate addiction are overstated; true opiate addiction is in fact rare.
Ten years or so ago if you pointed out narcotic seeking behavior you would be told, dismissively, that this was not addiction but pseudoaddiction. Pseudoaddiction, they said, was merely behavior exhibited by a patient whose pain was uncontrolled. Put another way, if your patient engaged in seeking behavior it meant you were not doing your job.
Pain can be measured.
Translate: pain is not subjective. Pain does not have emotional components. How many people knew that was a crock but were too intimidated to call it out?
No one should have to experience pain. Pain can be made to disappear from the planet.
Really? How about all those patients on chronic narcotics who have had their doses increased, time and time again, to ridiculously high levels, and are still suffering?
It's great to see that some people are finally saying enough is enough.
Saturday, November 15, 2014
Sgarbossa rule: not just for LBBB?
The Sgarbossa rule has been extrapolated to ventricular paced complexes. As illustrated in this post from Dr. Smith's ECG blog it can also be applied to ventricular ectopic complexes, as seen in AIVR. The post presents a fascinating case with a lot of teaching points.
Friday, November 14, 2014
Can medical students learn point of care echocardiography with brief training?
From a recent study:
Via Hospital Medicine Virtual Journal Club.
..The aim of this study was to assess the diagnostic value of bedside echocardiographic examinations performed with the use of pocket-size echocardiograph by experienced cardiologist and medical students...
All patients underwent bedside echocardiographic examination performed with pocket-size echocardiograph by two briefly trained medical students (n=90 patients) or cardiologist (n=30 patients). Major findings were recorded using a simplified questionnaire. Within 24 hours standard echocardiographic examination was performed in all patients by another cardiologist using a full sized echocardiograph. The study group was divided into 4 subgroups: A / B - first / second half of in-patients examined by students, group C - inpatients examined by cardiologist, group D- out-patients examined by students.
Results: The agreement between standard transthoracic echocardiography (sTTE) and major findings on bedside transthoracic echocardiography (bTTE) was fair to moderate (kappa 0.293-0.57) in group A, moderate to very good (kappa 0.535-1.00) in group B, good to very good (kappa 0.734-1.00) in group C and moderate to very good (kappa 0.590-1.00) in group D.
Conclusions: Pocket-size echocardiograph enables an expert echocardiographer to perform reliable bedside examinations. When used by briefly trained medical students it provides an acceptable diagnostic value with notable learning curve effect.
Via Hospital Medicine Virtual Journal Club.
Thursday, November 13, 2014
Primary hyperparathyroidism: sporadic versus MEN associated
There are important differences in disease characteristics and treatment approach. Review here.
Wednesday, November 12, 2014
Tuesday, November 11, 2014
Stress hyperglycemia in hospitalized patients and future risk of diabetes
From a recent retrospective cohort study:
In a retrospective cohort study, patients aged 30 years or older with an emergency admission to hospital between 2004 and 2008 were included. Prevalent and incident diabetes were identified through the Scottish Care Information (SCI)-Diabetes Collaboration national registry. Patients diagnosed prior to or up to 30 days after hospitalisation were defined as prevalent diabetes and were excluded.
The predicted risk of developing incident type 2 diabetes during the 3 years following hospital discharge by admission glucose, age, and sex was obtained from logistic regression models. We performed separate analyses for patients aged 40 and older, and patients aged 30 to 39 years.
Glucose was measured in 86,634 (71.0%) patients aged 40 and older on admission to hospital. The 3-year risk of developing type 2 diabetes was 2.3% (1,952/86,512) overall, was less than 1% for a glucose less than or equal to 5 mmol/l, and increased to approximately 15% at 15 mmol/l. The risks at 7 mmol/l and 11.1 mmol/l were 2.6% (95% CI 2.5–2.7) and 9.9% (95% CI 9.2–10.6), respectively, with one in four (21,828/86,512) and one in 40 (1,798/86,512) patients having glucose levels above each of these cut-points. For patients aged 30–39, the risks at 7 mmol/l and 11.1 mmol/l were 1.0% (95% CI 0.8–1.3) and 7.8% (95% CI 5.7–10.7), respectively, with one in eight (1,588/11,875) and one in 100 (120/11,875) having glucose levels above each of these cut-points.
The risk of diabetes was also associated with age, sex, and socio-economic deprivation, but not with specialty (medical versus surgical), raised white cell count, or co-morbidity. Similar results were obtained for pre-specified sub-groups admitted with myocardial infarction, chronic obstructive pulmonary disease, and stroke.
There were 25,193 deaths (85.8 per 1,000 person-years) over 297,122 person-years, of which 2,406 (8.1 per 1,000 person-years) were attributed to vascular disease. Patients with glucose levels of 11.1 to 15 mmol/l and greater than 15 mmol/l had higher mortality than patients with a glucose of less than 6.1 mmol/l (hazard ratio 1.54; 95% CI 1.42–1.68 and 2.50; 95% CI 2.14–2.95, respectively) in models adjusting for age and sex...
Conclusion
Plasma glucose measured during an emergency hospital admission predicts subsequent risk of developing type 2 diabetes. Mortality was also 1.5-fold higher in patients with elevated glucose levels. Our findings can be used to inform patients of their long-term risk of type 2 diabetes, and to target lifestyle advice to those patients at highest risk.
Monday, November 10, 2014
Mitral valve prolapse review
Another review of MVP recently appeared in Circulation. It makes many of the same points I made in my recent post on this topic. Some points for emphasis:
MVP may be genetic or sporadic.
The genetics remain poorly understood.
Some cases of MVP are associated with heritable disorders of connective tissue.
Those cases are referred to as syndromic MVP. Those not associated with another disorder are referred to as nonsyndromic. Among the heritable disorders of connective tissue the strongest association appears to be with Marfan syndrome.
There is a possible association with hypertrophic cardiomyopathy.
From the review:
Dysregulation of the autonomic nervous system has been cited as characteristic of MVP but the nature and significance of the association is unclear.
As I stated in my earlier post on this topic, laxity of older echocardiographic criteria for MVP in the 70s and early 80s led to overdiagnosis. Patients with other syndromes were lumped together with those who had true MVP. Many of those erroneously diagnosed as MVP were patients with a dysautonomia which has been known for over a century but referred to by different names over time, e.g. DaCosta’s syndrome, soldier’s heart, neurocirculatory aesthenia and, most recently postural orthostatic tachycardia syndrome (POTS). The degree of overlap of this syndrome with true MVP, if any, remains unclear.
MVP may be genetic or sporadic.
The genetics remain poorly understood.
Some cases of MVP are associated with heritable disorders of connective tissue.
Those cases are referred to as syndromic MVP. Those not associated with another disorder are referred to as nonsyndromic. Among the heritable disorders of connective tissue the strongest association appears to be with Marfan syndrome.
There is a possible association with hypertrophic cardiomyopathy.
From the review:
The largest study assessing the prevalence of MVP in HCM observed it in 3% (of 528 people with HCM), which might suggest that HCM and MVP are 2 distinct conditions that may coexist in some cases.53 However, the prevalence of other MV abnormalities (leaflet elongation and increased thickness) is much higher in HCM, estimated at 66% in 1 study.54 This suggests that MV abnormalities are intrinsic to HCM,54 either as a primary trait or as a secondary adaptive response to shear stress in a turbulent outflow tract or paracrine effects arising in the adjacent hypertrophic ventricle (see below).55
Dysregulation of the autonomic nervous system has been cited as characteristic of MVP but the nature and significance of the association is unclear.
As I stated in my earlier post on this topic, laxity of older echocardiographic criteria for MVP in the 70s and early 80s led to overdiagnosis. Patients with other syndromes were lumped together with those who had true MVP. Many of those erroneously diagnosed as MVP were patients with a dysautonomia which has been known for over a century but referred to by different names over time, e.g. DaCosta’s syndrome, soldier’s heart, neurocirculatory aesthenia and, most recently postural orthostatic tachycardia syndrome (POTS). The degree of overlap of this syndrome with true MVP, if any, remains unclear.
Sunday, November 09, 2014
Which patients in the hospital should receive stress ulcer prophylaxis?
Stress ulcer prophylaxis is not a publicly reported core measure or the focus of a government sponsored reimbursement incentive. It is, however, a de facto performance measure, having become embedded in many locally originated care pathways and bundles and consequently driven to excessive use.
Evidence based application of stress ulcer prophylaxis is much more restrictive than common practice. The topic is reviewed concisely in a recent article in Cleveland Clinic Journal of Medicine. From the article:
Evidence based application of stress ulcer prophylaxis is much more restrictive than common practice. The topic is reviewed concisely in a recent article in Cleveland Clinic Journal of Medicine. From the article:
Based on current evidence and guidelines, routine acid-suppressive therapy to prevent stress ulcers has no benefit in hospitalized patients outside the critical-care setting. Only critically ill patients who meet specific criteria, as described in the guidelines of the American Society of Health System Pharmacists, should receive acid-suppressive therapy...
The American Society of Health System Pharmacists guidelines recommend it in the intensive care unit for patients with any of the following: coagulopathy, prolonged mechanical ventilation (more than 48 hours), GI ulcer or bleeding within the past year, sepsis, a stay longer than 1 week in the intensive care unit, occult GI bleeding for 6 or more days, and steroid therapy with more than 250 mg of hydrocortisone daily.8 Hemodynamically stable patients admitted to general-care floors should not receive stress ulcer prophylaxis...
Saturday, November 08, 2014
Meta-analysis on neurologic prognosis post arrest
Recently published in Critical Care Medicine:
Data Synthesis: Of 2,737 citations, 20 studies (n = 1,845) met inclusion criteria. Meta-analysis showed that three tests accurately predicted poor neurologic outcome with low false-positive rates: bilateral absence of pupillary reflexes more than 24 hours after a return of spontaneous circulation (false-positive rate, 0.02; 95% CI, 0.01–0.06; summary positive likelihood ratio, 10.45; 95% CI, 3.37–32.43), bilateral absence of corneal reflexes more than 24 hours (false-positive rate, 0.04; 95% CI, 0.01–0.09; positive likelihood ratio, 6.8; 95% CI, 2.52–18.38), and bilateral absence of somatosensory-evoked potentials between days 1 and 7 (false-positive rate, 0.03; 95% CI, 0.01–0.07; positive likelihood ratio, 12.79; 95% CI, 5.35–30.62). False-positive rates were higher for a Glasgow Coma Scale motor score showing extensor posturing or worse (false-positive rate, 0.09; 95% CI, 0.06–0.13; positive likelihood ratio, 7.11; 95% CI, 5.01–10.08), unfavorable electroencephalogram patterns (false-positive rate, 0.07; 95% CI, 0.04–0.12; positive likelihood ratio, 8.85; 95% CI, 4.87–16.08), myoclonic status epilepticus (false-positive rate, 0.05; 95% CI, 0.02–0.11; positive likelihood ratio, 5.58; 95% CI, 2.56–12.16), and elevated neuron-specific enolase (false-positive rate, 0.12; 95% CI, 0.06–0.23; positive likelihood ratio, 4.14; 95% CI, 1.82–9.42). The specificity of available tests improved when these were performed beyond 72 hours. Data on neuroimaging, biomarkers, or combination testing were limited and inconclusive.
Conclusion: Simple bedside tests and somatosensory-evoked potentials predict poor neurologic outcome for survivors of cardiac arrest treated with targeted temperature management, and specificity improves when performed beyond 72 hours. Clinicians should use caution with these predictors as they carry the inherent risk of becoming self-fulfilling.
Friday, November 07, 2014
Adherence to the Surviving Sepsis Campaign bundles
---decreased mortality in this study. Similar evidence of improved outcomes attributable to the campaign has been reported previously. The campaign, by the way, has been lambasted by the pharmascolds as stealth marketing and a marketing campaign disguised as evidence based medicine.
Thursday, November 06, 2014
MD Consult is going away
--- and being replaced by Clinical Key.
This review was negative. I have tried Clinical Key and found it, like MD Consult, to be a decent product although it is apparently more expensive. It is essentially a re-branding by Elsevier of MD Consult with a few bells and whistles and additional journals added. I don't know why they made this decision when MD Consult performed so well at what it was supposed to do. The interface has a new look and appears more geared to searching as opposed to browsing, suggesting a move to be more of a point of care reference for evidence based searching as opposed to an electronic version of the traditional medical library, which was MD Consult's strength.
UpToDate and DynaMed are examples of point of care look-up sites. They are well designed for getting quick answers to focused clinical questions in real time. MD Consult and Clinical Key are less suited for that purpose. Clinical Key's search engine, although powerful and even fun, is imprecise. It searches across a vast array of sources but they are diverse and not filtered in any systematic way as far as I can tell. Search results tend to be random, almost luck of the draw. While searching in that manner can be productive it is not systematic or rigorous according to the standards of EBM. Resources like this are great for background reading such as you might do during down time when you want to dive deep about your patient's disease process. They are less useful when trying to quickly answer focused clinical questions. I use UpToDate to get fast, focused answers during patient care. It is possible though more difficult to use it for background reading. If you use UpToDate to try and assemble something akin to a monograph or a textbook chapter you'll be jumping from page to page and may get lost in what seems an endless trail of links.
A sharp distinction needs to be made. Point of care sites such as UpToDate and DynaMed differ from electronic libraries like MD Consult, Clinical Key and Access Medicine. Confusion results when the distinction is lost. You can use either type of resource for either purpose but certainly UpToDate is optimized for one type of research and MD Consult and Clinical Key for another. No single site works well in both areas.
If Clinical Key is trying to compete with UpToDate it's the wrong focus. Clinicians need both types. They are complementary and neither should replace the other. Several years ago I wrote a post about these two uses of on line resources, reflecting the two distinct reading objectives. In that post I borrowed a couple of terms I had heard form a speaker somewhere: background reading and foreground reading.
This review was negative. I have tried Clinical Key and found it, like MD Consult, to be a decent product although it is apparently more expensive. It is essentially a re-branding by Elsevier of MD Consult with a few bells and whistles and additional journals added. I don't know why they made this decision when MD Consult performed so well at what it was supposed to do. The interface has a new look and appears more geared to searching as opposed to browsing, suggesting a move to be more of a point of care reference for evidence based searching as opposed to an electronic version of the traditional medical library, which was MD Consult's strength.
UpToDate and DynaMed are examples of point of care look-up sites. They are well designed for getting quick answers to focused clinical questions in real time. MD Consult and Clinical Key are less suited for that purpose. Clinical Key's search engine, although powerful and even fun, is imprecise. It searches across a vast array of sources but they are diverse and not filtered in any systematic way as far as I can tell. Search results tend to be random, almost luck of the draw. While searching in that manner can be productive it is not systematic or rigorous according to the standards of EBM. Resources like this are great for background reading such as you might do during down time when you want to dive deep about your patient's disease process. They are less useful when trying to quickly answer focused clinical questions. I use UpToDate to get fast, focused answers during patient care. It is possible though more difficult to use it for background reading. If you use UpToDate to try and assemble something akin to a monograph or a textbook chapter you'll be jumping from page to page and may get lost in what seems an endless trail of links.
A sharp distinction needs to be made. Point of care sites such as UpToDate and DynaMed differ from electronic libraries like MD Consult, Clinical Key and Access Medicine. Confusion results when the distinction is lost. You can use either type of resource for either purpose but certainly UpToDate is optimized for one type of research and MD Consult and Clinical Key for another. No single site works well in both areas.
If Clinical Key is trying to compete with UpToDate it's the wrong focus. Clinicians need both types. They are complementary and neither should replace the other. Several years ago I wrote a post about these two uses of on line resources, reflecting the two distinct reading objectives. In that post I borrowed a couple of terms I had heard form a speaker somewhere: background reading and foreground reading.
What are the high risk electrocardiographic features in patients presenting with syncope?
Know them. This topic discussion provides some illustrative tracings.
Wednesday, November 05, 2014
Dexmedetomidine as an adjunct for alcohol withdrawal: non-evidence based but promising
Dexmedetomidine for treatment of alcohol withdrawal has appealing properties but is off label and one of the most non-evidence based practices in intensive care medicine. But this small study is promising:
Materials and Methods
This retrospective case series evaluated 33 critically ill adults with a primary diagnosis of AWS from 2006 to 2012 at an academic medical center.
Results
Dexmedetomidine began a median (interquartile range) of 11 (2, 32) hours into intensive care unit admission and was titrated to an infusion rate of 0.7 (0.4, 0.7) μg kg−1 h−1 to achieve the desired depth of sedation. In the 12 hours after dexmedetomidine began, patients experienced a 20-mg reduction in median cumulative benzodiazepine dose used (P less than .001), a 14-mm Hg lower mean arterial pressure (P = .03), and a 17-beats/min reduction in median heart rate (P less than .001). Four (12%) patients experienced hypotension (systolic blood pressure less than 80 mm Hg) during therapy, and there were no cases of bradycardia (heart rate less than 40 beats/min).
Conclusion
Dexmedetomidine decreased benzodiazepine requirements and improved the overall hemodynamic profile of patients with severe AWS. These results provide promising evidence about the potential benefit of dexmedetomidine for AWS.
Secondary hypertension endocrinopathies
From a recent review:
Endocrine hypertension is an important secondary form of hypertension, identified in between 5% and 10% of general hypertensive population. Primary aldosteronism is the most common cause of endocrine hypertension, accounting for 1%–10% in uncomplicated hypertension and 7%–20% in resistant hypertension. Other less common causes of endocrine hypertension include Cushing syndrome, pheochromocytoma, thyroid disorders, and hyperparathyroidism.
Tuesday, November 04, 2014
Critical care reviews
From the home page:
Critical Care Reviews is a free, not-for-profit, educational critical care resource run by Rob Mac Sweeney, an intensivist in Belfast, Northern Ireland. The site offers many resources, including a journal watch facility, weekly newsletter, the largest structured collection of accessible critical care review articles on the internet, links to major studies and guidelines, as well as links to free vodcasts, podcasts, and a vast array of societies, groups and websites. Continuing Professional Development articles are provided, as are links to exam resources. In addition to the content on the site, Critical Care Reviews is hosting a meeting in January 2014, discussing the major studies of 2013.
Monday, November 03, 2014
More on the resuscitation fluid debate
The debate surrounding resuscitation fluid is heating up. I previously blogged about a review in NEJM here. A similar review appeared in the World Journal of Critical Care Medicine and is available as free full text. Below are some key issues from that review.
Assessing the need for fluid and monitoring the response
Traditional metrics such as CVP have recently been called into question. Novel approaches such as pulse pressure variation and echocardiographic assessment of IVC diameter and its respiratory variation are believed to be superior but supported mainly by low level data. How do we know that once subject to rigorous outcome based trials they won't go the way of the PA catheter? On the other hand the article points out that there is some value in measurement of tissue perfusion end points such as lactate. So, although how to assess volume is controversial, volume assessment remains important. Good old fashioned bedside clinical assessment, perhaps guided by lactate measurements, may be as good as anything we can do. Individualization of therapy is more important than, as termed in the paper, “generic resuscitation endpoints.”
Crystalloid versus colloid
This debate remains unsettled. We lack strong evidence that colloid, which is more expensive, is any better than crystalloid. The recently published ALBIOS trial raised interest in the use of albumin in severe sepsis and septic shock. However, this was not a comparative study of resuscitation fluids and the results were mixed. For a balanced discussion of ALBIOS see here. Finally, keep in mind special situations in which albumin is specifically recommended such as hepatorenal syndrome and spontaneous bacterial peritonitis. The harm associated with starch products is well known and has been discussed previously.
Which crystalloid?
The past couple of years have seen a rising concern over whether balanced electrolyte solutions should be used instead of normal saline. Balanced solutions have long had theoretical appeal. More recently data are trickling in suggesting that balanced solutions are associated with better outcomes. Though not strong enough to mandate practice change they do warrant consideration in the choice of crystalloid in various situations.
How much fluid?
Recent findings suggest that the answer is time dependent. Under resuscitation is a concern in the early hours. However, net positive fluid balance over a longer period appears harmful. Stated simply, front load then back off. The authors of the review take it a step further by suggesting a third phase of active fluid removal later in the course of illness.
Assessing the need for fluid and monitoring the response
Traditional metrics such as CVP have recently been called into question. Novel approaches such as pulse pressure variation and echocardiographic assessment of IVC diameter and its respiratory variation are believed to be superior but supported mainly by low level data. How do we know that once subject to rigorous outcome based trials they won't go the way of the PA catheter? On the other hand the article points out that there is some value in measurement of tissue perfusion end points such as lactate. So, although how to assess volume is controversial, volume assessment remains important. Good old fashioned bedside clinical assessment, perhaps guided by lactate measurements, may be as good as anything we can do. Individualization of therapy is more important than, as termed in the paper, “generic resuscitation endpoints.”
Crystalloid versus colloid
This debate remains unsettled. We lack strong evidence that colloid, which is more expensive, is any better than crystalloid. The recently published ALBIOS trial raised interest in the use of albumin in severe sepsis and septic shock. However, this was not a comparative study of resuscitation fluids and the results were mixed. For a balanced discussion of ALBIOS see here. Finally, keep in mind special situations in which albumin is specifically recommended such as hepatorenal syndrome and spontaneous bacterial peritonitis. The harm associated with starch products is well known and has been discussed previously.
Which crystalloid?
The past couple of years have seen a rising concern over whether balanced electrolyte solutions should be used instead of normal saline. Balanced solutions have long had theoretical appeal. More recently data are trickling in suggesting that balanced solutions are associated with better outcomes. Though not strong enough to mandate practice change they do warrant consideration in the choice of crystalloid in various situations.
How much fluid?
Recent findings suggest that the answer is time dependent. Under resuscitation is a concern in the early hours. However, net positive fluid balance over a longer period appears harmful. Stated simply, front load then back off. The authors of the review take it a step further by suggesting a third phase of active fluid removal later in the course of illness.
Does tramadol cause seizures?
There's a nice evidence summary over at Emergency Medicine PharmD which concludes:
In summary, the risk of seizures in patients taking tramadol alone appears to be equal to patients not taking tramadol. However, certain risk factors may contribute to an increased risk of seizures in patients receiving tramadol. Co-morbid conditions predisposing patients to seizures, alcohol use and/or abuse, TCAs, SSRIs, MAOIs, other opiate use, other antidepressants and other drugs that may reduce the seizure threshold in conjunction with tramadol use have been associated with increased incidence of seizures. In addition, chronic users and abusers of tramadol seem to be at an increased risk of seizures.
Sunday, November 02, 2014
Initial lactate levels and lactate clearance post cardiac arrest
An observational study from the National Post-Arrest Research Consortium:
The primary outcome was survival to hospital discharge, and secondary outcome was good neurologic outcome. We compared the absolute lactate levels and the differences in the percent lactate change over 24 hours between survivors and nonsurvivors and between subjects with good and bad neurologic outcomes. One hundred patients were analyzed. The median age was 63 years (interquartile range, 50–75) and 40% were female. Ninety-seven percent received therapeutic hypothermia, and overall survival was 46%. Survivors and patients with good neurologic outcome had lower lactate levels at 0, 12, and 24 hours (p less than 0.01). In adjusted models, percent lactate decrease at 12 hours was greater in survivors (odds ratio, 2.2; 95% CI, 1.1–6.2) and in those with good neurologic outcome (odds ratio, 2.2; 95% CI, 1.1–4.4).
Conclusion: Lower lactate levels at 0, 12, and 24 hours and greater percent decrease in lactate over the first 12 hours post cardiac arrest are associated with survival and good neurologic outcome.
Overextension of IC antiarrhythmic contraindications due to overhype of CAST
Saturday, November 01, 2014
Left atrial appendage closure
From the conclusion of a recent review in Circulation:
The report also cites a smaller trial which failed to establish non-inferiority of the device over anticoagulation, but noted a remarkably low event rate in the anticoagulation group.
Although the mechanism of thromboembolism in AF is multifactorial, the LAA appears to be the major source of thrombus and is a target for transcatheter interventional therapy with device occlusion or ligation. The WATCHMAN has the largest data set for clinical end points, having been evaluated in 2 randomized trials and an FDA-monitored continuing-access registry in warfarin-eligible patients. In total, these studies support the clinical efficacy of the WATCHMAN in preventing thromboembolic events in the absence of anticoagulation and, in turn, provide mechanistic support for the concept of LAA closure for stroke prevention in at-risk patients. However, extrapolating these findings to other LAA devices is perilous because there are limited safety data and a paucity of robust clinical outcomes data for alternative approaches to LAA closure. Patient selection for the WATCHMAN device should be guided by an assessment of thromboembolic and bleeding risk, in addition to patient preference.
The report also cites a smaller trial which failed to establish non-inferiority of the device over anticoagulation, but noted a remarkably low event rate in the anticoagulation group.
What's the ideal IV fluid?
Here's a review from Current Opinion in Critical Care Medicine.
Take home messages:
The colloid versus crystalloid debate remains unsettled.
Starch preparations are to be discouraged.
Among crystalloid solutions an emerging literature favors balanced solutions over saline. This however needs to be confirmed in higher level studies.
From the review:
Take home messages:
The colloid versus crystalloid debate remains unsettled.
Starch preparations are to be discouraged.
Among crystalloid solutions an emerging literature favors balanced solutions over saline. This however needs to be confirmed in higher level studies.
From the review:
Intravenous fluids, historically described as crystalloids or colloids, are administered with the aim of maintaining acceptable cardiac output and preserving the microcirculation. Achieving the aim of fluid administration is impacted by alterations in vascular permeability in critically ill patients. There is a strong body of evidence demonstrating the harmful effects of HES preparations, specifically regarding tissue storage with associated adverse renal, hepatic, cutaneous and haematological outcomes. The use of human colloids is limited by resource constraints, infectious and noninfectious risks. Hyperchloraemia, a well documented undesirable effect from administration of 0.9% saline, currently the most commonly prescribed crystalloid, is proinflammatory and is associated with increased morbidity and mortality. Not only is there no generic fluid that will cover all circumstances, but no ideal fluid exists for any specific situation. Further research comparing 0.9% saline to a balanced salt solution may reveal a type of fluid that is the closest to being ideal.
Ulcerative colitis
If there was such a thing as an article that could make you an expert on ulcerative colitis this would be it. It has a lot of great pearls and belongs in every internist's library. I won't list the pearls here because free full text is available at the link and the article should be read in its entirety.
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