From a recently published cohort study:
Patients: Veterans who initiated metformin or sulfonylurea therapy for diabetes. Patients with chronic kidney disease or serious medical illness were excluded.
Measurements: Composite outcome of hospitalization for acute myocardial infarction or stroke, or death...
...crude rates of the composite outcome were 18.2 per 1000 person-years in sulfonylurea users and 10.4 per 1000 person-years in metformin users (adjusted incidence rate difference, 2.2 [95% CI, 1.4 to 3.0] more CVD events with sulfonylureas per 1000 person-years; adjusted hazard ratio [aHR], 1.21 [CI, 1.13 to 1.30]). Results were consistent for both glyburide (aHR, 1.26 [CI, 1.16 to 1.37]) and glipizide (aHR, 1.15 [CI, 1.06 to 1.26]) in subgroups by CVD history, age, body mass index, and albuminuria; in a propensity score–matched cohort analysis; and in sensitivity analyses.
According to the authors and the editors it cannot be said whether metformin confers macrovascular benefit, sulfonylureas cause macrovascular harm or both. In the 1970s the University Group Diabetes Program (UGDP) study showed macrovascular harm attributable to sulfonylurea therapy and the class of agents has since carried a black box warning. The UKPDS also suggested superior outcomes with metformin including specifically the macrovascular outcome of stroke.
The authors of the cohort study cite other prior research suggesting superiority of metformin, particularly for macrovascular outcomes, despite similarity in glycemic control compared to other agents.
The emerging picture is that for microvascular disease the more you lower blood sugar the better, no matter how. For macrovascular disease this does not hold true in simple fashion. If lowering blood sugar does matter, it matters how and with what.
There is more and more coming out about this. Recently the green journal published Pneumonia: An Arrhythmogenic Disease?
Background
Recent studies suggest that there is an increase in cardiovascular disease after pneumonia; however, there is little information on cardiac arrhythmias after pneumonia. The aims of this study were to assess the incidence of, and examine risk factors for, cardiac arrhythmias after hospitalization for pneumonia.
Methods
We conducted a national cohort study using Department of Veterans Affairs administrative data including patients aged greater than or equal to 65 years hospitalized with pneumonia in fiscal years 2002-2007, receiving antibiotics within 48 hours of admission, having no prior diagnosis of a cardiac arrhythmia, and having at least 1 year of Veterans Affairs care...
Results
We identified 32,689 patients who met the inclusion criteria. Of these, 3919 (12%) had a new diagnosis of cardiac arrhythmia within 90 days of admission. Variables significantly associated with increased risk of cardiac arrhythmia included increasing age, history of congestive heart failure, and a need for mechanical ventilation or vasopressors. Beta-blocker use was associated with a decreased incidence of events.
Conclusion
An important number of patients have new cardiac arrhythmia during and after hospitalization for pneumonia. Additional research is needed to determine whether use of cardioprotective medications will improve outcomes for patients hospitalized with pneumonia. At-risk patients hospitalized with pneumonia should be monitored for cardiac arrhythmias during the hospitalization.
(My italics above).
Additional reading:
Aspirin to decrease adverse cardiac events in pneumonia patients.
Sudden cardiac death in pneumonia and other infections.
Review in American Family Physician.
This study found a 1 year increase in mortality in discharged elders, attributable mainly to high dose PPI use. PPIs are great drugs but they must be used discriminately. Overuse may be driven by the belief that these drugs are benign, consumer demand and poorly conceived care bundles resulting in inappropriate prescribing for “GI prophylaxis.” The mechanisms of harm are gradually being discovered. See here.
Though hospitalist programs have long relied heavily on locums and continue to do so, increasing controversy surrounds the practice according to this article in Today's Hospitalist. Staffing company and hospitalist program leaders interviewed for the article say the difficult issues are the high cost of hiring locum doctors, instability of group culture and perceived quality problems. Quality issues are not necessarily inherent in the locum doctor, as many excellent hospitalists see locum work as an opportunity for flexibility and better compensation. But even great locum docs may look inferior on various metrics (artificial quality surrogates) because they lack a sense of group ownership and are not under institutional performance incentives. Part of the appeal of locum tenens work may be a sense of freedom from performance pressure.
If hospitalist groups intend to rely less on staffing companies as some leaders claim the trade off is to look to other sources of temporary help such as within-the-group moonlighting. No matter how you slice it staffing shortages remain critical and there's no sign of relief, making me wonder if last year's downtick in hospitalist compensation was an anomaly.
Good on prevention, not so good if you get sick. The authors of this NEJM piece seem to like it but don't romanticize it, they say. OK. From the article:
The system is not designed for consumer choice or individual initiatives. There is no alternative, private-payer health system. Physicians get government benefits such as housing and food subsidies, but they are paid only about $20 per month. Their education is free, and they are respected, but they are unlikely to attain personal wealth. Cuba is a country where 80% of the citizens work for the government, and the government manages the budgets...
A nephrologist in Cienfuegos, 160 miles south of Havana, lists 77 patients on dialysis in the province, which on a population basis is about 40% of the current U.S. rate — similar to what the U.S. rate was in 1985. A neurologist reports that his hospital got a CT scanner only 12 years ago. U.S. students who are enrolled in a Cuban medical school say that operating rooms run quickly and efficiently but with very little technology. Access to information through the Internet is minimal. One medical student reports being limited to 30 minutes per week of dial-up access.
The authors suggest that's the result of the U.S. Economic embargo.
----think beyond the valve. It's really a disease of the entire aorta. From the review:
A more recent study has looked at the incidence of aortic complications in 416 BAV patients (mean and median age 35 years, range less than 1–89) [32]. Incidence of aortic dissection was found to be 1.5% in all patients regardless of the progression of BAV; however this increased markedly in patients aged 50 or older at baseline to 17.4% and even more in those found to have aneurysm formation at baseline to (44.9%). 25-year rate for aortic surgery was 25% and there was a significant burden of progression of disease to cause aortic dissection with 49 of the 384 patients without baseline aneurysms developing them during followup, giving an age-adjusted relative risk of 86.2 and an incidence of 84.9 cases per 10000 patient-years.
I should know because I was involved in the movement nearly from the beginning. Back then the distinctive was that hospitalists were doctors who, having ascended a steep learning curve from practicing exclusively inpatient medicine, had a special degree of expertise and skill to meet the challenges of caring for the incredibly ill and complex patients who populate the hospital. In short, we were (once) valued for our clinical skills.
Right in line with this was the understanding that effective use of such skills would require enough time to spend with each patient. After all being a good clinician takes time. Practicing evidence based medicine takes time. This led early programs to define who and what they were clinically and to carefully structure coverage arrangements with appropriate restrictions. No one in their wildest imagination had any notion of taking over the hospital or admitting for everyone. At least not in the beginning. But hospitalist leaders started planting the seeds of that idea a few years ago.
I saw trouble brewing then and have blogged my concern many times since. I once made fun of the trend I observed as the hospitalist role was devalued and transitioned from expert clinician to utility player:
Hospitalist skill set, year 2000:
Management of CAP and HCAP
Management of sepsis
Management of venous thromboembolism
Management of DKA, adrenal crisis and other endocrine-metabolic emergencies
Management of COPD, asthma and ARDS, including ventilator management
Management of renal, fluid and electrolyte problems
Management of acute decompensated heart failure
Management of toxicologic emergencies
Providing consultation for complex and difficult diagnostic problems
Providing consultation for medical complications in surgical, subspecialty and general medical patients
Hospitalist skill set, year 2010:
Tweaking Press Ganey
Tweaking clinical documentation (DRGs)
Creative coding
Bed control
Admitology, roundology and dischargology for surgical and subspecialty patients
Cosmetic charting (performance measures)
Secretarial (CPOE)
So I recently found another published example of the trend in a recent issue of Today's Hospitalist: Universal admitters: hospitalists' new identity? The article cites the growing trend of hospitalists admitting nearly all comers regardless of the clinical need. This according to the article off-loads the specialists, expands the hospitalist's niche and serves the business needs of the institution. Several program leaders were interviewed. To their credit they paid lip service to the concerns about hospitalists becoming overburdened or taking on duties outside the scope of their training. Ultimately, though, to my disappointment, they seemed to one degree or another complicit with the new agenda.
For example:
"The greatest difficulty for hospitalist groups is not recognizing the value in being on the front lines of caring for the majority of patients," Dr. Bossard says. "Going into meetings with the idea that we're going to try to protect our turf and reduce the number of patients we carry by establishing rules to protect us won't work."
I have a little different view of protecting turf. If only the specialty services would protect their own turf! But they seem eager to give it up while hospitalists at the organizational level seem all to willing to capitulate and take it on.
Clinical skill has all but vanished as the raison d'etre for hospitalists. And in the article it's missing from the discussion of all the things the hospitalist “brings to the table,” for example computer skills:
Another factor driving hospitalists toward more admissions: Subspecialists are frustrated with electronic medical records. It makes sense to hand off the computer work associated with being the admitting physician to hospitalists, who log in much more screen time.
Though mentioned as an aside that paragraph says a lot about the changing agenda: the move toward hospitalist as secretary, H&P provider and off-loader.
Once an open access journal, American Family Physician for the past few years has been behind heavy access controls. Every once in a while a really good review shows up there. Recently they published this article on Guillain-Barré syndrome. It is worth reading in the full text if you can get it.
Some points of interest:
Though the varied spectrum of GBS has enough important features in common to discuss for practical purposes as a single entity it is probably best thought of as a group of diseases reflecting the different immune responses, different targets of immune injury (myelin vs axon), differences in epidemiology and the clinical variants.
Pain and autonomic instability are very common features, I think more than generally appreciated. So maybe you've got a patient presenting with funny unexplained pains and vital signs all over the map. Maybe with multiple preceding ER visits. Think of it!
Symptoms are bilateral and tend to be symmetric but may not be perfectly so at all points in the clinical course.
Reflexes have to be decreased but not necessarily absent at all points in the clinical course.
The epidemiology is complex. While often discussed in the context of Campylobacter jejuni, that infection is associated with a variant of GBS (axonal) not typical in the U.S. A variety of illnesses may precede GBS.
There are two arms of treatment: supportive and disease specific.
Supportive care addresses DVT prophylaxis, pain control, skin care, bowel and bladder issues, physical therapy, cardiac and vital sign monitoring and respiratory care. Multiple respiratory parameters can be monitored. The article lists, among other signs, forced vital capacity less than 20 mL/kg, maximum inspiratory pressure less than 30 cmH2O, and maximum expiratory pressure less than 40 cmH2O as risk factors for respiratory failure. The presence of any of the three signs, according to Up to Date, is an indication for urgent intubation and mechanical ventilation.
Disease specific modalities are plasma exchange and IVIG. One or the other is used, not both. Is one preferred over the other? The review article says plasma exchange is “first line.” The Up to Date section on treatment of GBS says the treatments are equivalent, and that IVIG tends to be favored due to availability and ease of use.
A recent paper reports a survey of state medical boards as to how they would respond to hypothetical scenarios:
High consensus was defined as more than 75% of respondents indicating that investigation was “likely” or “very likely,” moderate consensus as 50% to 75% indicating this, and low consensus as fewer than 50% indicating this.
Four online vignettes demonstrated high consensus: Citing misleading information about clinical outcomes (81%; 39/48), using patient images without consent (79%; 38/48), misrepresenting credentials (77%; 37/48), and inappropriately contacting patients (77%; 37/48). Three demonstrated moderate consensus for investigation: depicting alcohol intoxication (73%; 35/48), violating patient confidentiality (65%; 31/48), and using discriminatory speech (60%; 29/48). Three demonstrated low consensus: using derogatory speech toward patients (46%; 22/48), showing alcohol use without intoxication (40%; 19/48), and providing clinical narratives without violation of confidentiality (16%; 7/48).
In this study transient ECG abnormalities were seen around the time of the episode of pneumonia. Some resembled those seen in PE.
---after two more trials published in NEJM here and here.
There were problems with the data, leaving open the possibility of benefit. But it remains unproven. Perspective here via Medpage Today.
---was formerly known as diastolic heart failure. A recent paper was published in the American Journal of Medicine: Contemporary Prevalence and Correlates of Incident Heart Failure with Preserved Ejection Fraction:
Background
We assessed the prevalence of preserved left ventricular ejection fraction in patients with incident heart failure and differences in the demographic and clinical characteristics that may differentiate patients presenting with heart failure with preserved versus reduced left ventricular ejection fraction.
Methods
We identified all patients with newly diagnosed heart failure between 2005 and 2008 from 4 sites in the Cardiovascular Research Network on the basis of hospital discharge and ambulatory visit diagnoses, and assigned a category of preserved, borderline, or reduced left ventricular ejection fraction using data from electronic databases and chart review.
Results
We identified 11,994 patients with incident heart failure; of these, 6210 (51.8%) had preserved left ventricular ejection fraction, 1870 (15.6%) had borderline systolic dysfunction, and 3914 (32.6%) had reduced left ventricular ejection fraction.
The authors list these key points:
•Heart failure with preserved left ventricular ejection fraction is the most common form of the heart failure syndrome among patients newly presenting with this condition.
•Women and older adults are especially affected.
•Patients with ejection fractions less than 40% comprise less than one third of those with incident heart failure.
•Evidence-based treatment strategies apply to only a minority of patients with newly diagnosed heart failure.
What does that last statement mean? Treatments have been validated by high level evidence for long term clinical outcomes (for the most part treatments with life prolonging neurohumoral antagonists) only for patients with clearly reduced ejection fractions. But those patients made up less than one third of the incident heart failure cases in this database. There's a commonly held maxim that “there is no evidence-based treatment available for HFPEF.” That's not exactly true. While there's no generalized treatment for the disease per se there are treatments for its manifestations (diuretics for pulmonary edema, rate controlling medications for atrial fibrillation) as well as its associated risk factors and comorbidities. These are, indeed, evidence-based and they treat the patient more than the disease.
According to this review it is emerging as a core skill for critical care docs. Will it be such for hospitalists??
From the review:
In recent years, several focused echocardiography protocols have been introduced [12]. These studies can usually be carried out by novice operators after a modest amount of training.
There's hope!
A case report and brief review of glucagonoma is presented here along with a discussion of a few other entities that can produce the same dermatosis. Free full text.
A concise review centering around a case report.
Misconceptions about Lyme disease abound and have fueled politicized debates and a good deal of quackery. A recent piece in the green journal (free full text) provides some clarity and includes a list of bullet points about the misconceptions. Here are a few:
Myth:
“'Blood tests are unreliable with many negatives in patients who really have Lyme disease'”
Fact:
“Just as with all antibody-based testing, these are often negative very early before the antibody response develops (less than 4-6 weeks). They are rarely if ever negative in later disease.”
Myth:
“'Antibiotics make blood tests negative during treatment'”
Fact:
“There is no evidence that this happens and no biologic reason it would.”
Myth:
“'Lyme disease is a clinical diagnosis that should be made based on a list of symptoms'”
Fact:
“No clinical features, except erythema migrans or possibly bilateral facial nerve palsy—in the appropriate context—provide sufficient specificity or positive predictive value. Laboratory confirmation is essential except with erythema migrans.”
Myth:
“'B. burgdorferi infection is potentially lethal'”
Fact:
“Although Lyme disease can cause heart or brain abnormalities, there have been remarkably few—if any—deaths attributable to this infection”
Myth:
“'If, following treatment, symptoms persist, or serologic testing remains positive, additional treatment is required'”
Fact:
“Multiple well-performed studies demonstrate that recommended treatment courses cure this infection. Retreatment is necessary occasionally, but not frequently.”
Now as readers know I'm not a fan of the Institute of Medicine (IOM) but they are quoted in the article and I happen to agree with what they said:
...strong emotions, mistrust, and a game of blaming others who are not aligned with one's views” have resulted in a heated and politicized debate. A number of factors have contributed to this “debate”—perhaps not the least of which is a tension between the concept of evidence-based medicine and medicine's historical inductive approach from anecdotal observation. This tension is reflected in 2 frequently repeated, interrelated assertions—that laboratory testing for Lyme disease is unreliable and that the disease should be defined “clinically”—meaning syndromically.
Much of this review is applicable to the EP lab although it contains some updated information on the surface ECG and how it can help in differentiating AVNRT from other SVTs.
From an article in the American Journal of Emergency Medicine:
A total of 1947 ED patients were enrolled; 192 (10%) were taking metformin; 305 (16%) died within 28 days. Metformin users had higher median lactate levels than nonusers (2.2 mmol/L [interquartile range, 1.6-3.2] vs 1.9 mmol/L [interquartile range, 1.3-2.8]) and a higher, although nonsignificant, prevalence of hyperlactatemia (lactate greater than or equal to 4.0 mmol/L) (17% vs 13%) (P = .17). In multivariate analysis (reference group nonmetformin users, lactate less than 2.0 mmol/L), hyperlactatemia was associated with an increased adjusted 28-day mortality risk among nonmetformin users (odds ratio [OR], 3.18; P less than .01) but not among metformin users (OR, 0.54; P = .33). In addition, nonmetformin users had a higher adjusted mortality risk than metformin users (OR, 2.49; P less than .01). These differences remained significant when only diabetic patients were analyzed.
Conclusions
In this study of adult ED patients with suspected sepsis, metformin users had slightly higher median lactate levels and prevalence of hyperlactatemia. However, hyperlactatemia did not predict an increased mortality risk in patients taking metformin.
According to a recent systematic review:
Results
Thirty reports describing 58 cases (41 preparations containing sorbitol and 17 preparations without sorbitol) of adverse events were identified. The colon was the most common site of injury (n=44; 76%), and transmural necrosis (n=36; 62%) was the most common histopathologic lesion reported. Mortality was reported in 33% of these cases due to gastrointestinal injury.
Conclusions
Sodium polystyrene sulfonate use, both with and without sorbitol, may be associated with fatal gastrointestinal injury. Physicians must be cognizant of the risk of these adverse events when prescribing this therapy for the management of hyperkalemia.
The only proven indication for PEEP is hypoxemia that is refractory to reasonable fractions of inspired oxygen. Yet, “five of PEEP” has become a default setting in mechanical ventilation no matter what the indication due to physiologic rationale and tradition. If cardiac decompensation (cardiogenic pulmonary edema) is in the loop of respiratory failure the physiologic rationale becomes even stronger because positive pressure applied anytime during the breathing cycle decreases afterload and has other hemodynamic benefits. That was the subject of this recent paper. The evidence is scant but PEEP appears to be safe and may offer clinical benefit when cardiac decompensation causes or complicates respiratory failure.
Here is an update in the American Journal of Emergency Medicine. Both the congenital and acquired forms are discussed. For congenital LQTS beta blockers are mentioned as first line therapy. The general principle guiding this recommendation is based on two different types of triggers for Torsades in patients with long QT: sympathetic surge (generally seen in the congenital form) and increased cardiac cycle length in the form of pause or bradycardia (the usual trigger in acquired cases). Overlap exists, however. Some acquired cases represent a mutation with weak expression, the phenotype manifesting for the first time in the face of an external factor such as an electrolyte disturbance or drug effect. And while the majority of genotypes respond to beta blockers some may not. The usual role of the hospitalist is to recognize abnormal repolarization in its various forms and address external triggers such as drugs and electrolyte disturbances, and know when to call the electrophysiologist.
From a recent paper in JAMA Internal Medicine:
Methods We conducted a retrospective, observational, inception cohort study of patients 18 years or older from 17 health plans participating in the Mini-Sentinel program who had initiated the use of an ACEI (n = 1 845 138), an ARB (n = 467 313), aliskiren (n = 4867), or a β-blocker (n = 1 592 278) between January 1, 2001, and December 31, 2010. We calculated the cumulative incidence and incidence rate of angioedema during a maximal 365-day follow-up period. Using β-blockers as a reference and a propensity score approach, we estimated the hazard ratios of angioedema separately for ACEIs, ARBs, and aliskiren...
The cumulative incidences per 1000 persons were 1.79 (95% CI, 1.73-1.85) cases for ACEIs, 0.62 (95% CI, 0.55-0.69) cases for ARBs, 1.44 (95% CI, 0.58-2.96) cases for aliskiren, and 0.58 (95% CI, 0.54-0.61) cases for β-blockers. The incidence rates per 1000 person-years were 4.38 (95% CI, 4.24-4.54) cases for ACEIs, 1.66 (95% CI, 1.47-1.86) cases for ARBs, 4.67 (95% CI, 1.88-9.63) cases for aliskiren, and 1.67 (95% CI, 1.56-1.78) cases for β-blockers. Compared with the use of β-blockers, the adjusted hazard ratios were 3.04 (95% CI, 2.81-3.27) for ACEIs, 1.16 (95% CI, 1.00-1.34) for ARBs, and 2.85 (95% CI, 1.34-6.04) for aliskiren.
Conclusions Compared with β-blockers, ACEIs or aliskiren was associated with an approximately 3-fold higher risk for angioedema, although the number of exposed events for aliskiren was small. The risk for angioedema was lower with ARBs than with ACEIs or aliskiren.
From the American Journal of Emergency Medicine:
Results
A total of 92 patients were enrolled in the study. Patients were divided into 2 groups based on whether they were treated (group1, n = 30) or not treated (group 2, n = 62) with sodium bicarbonate. There were no significant differences in demographic characteristics between groups. The median time interval between the administration of CPR and sodium bicarbonate injection was 36.0 minutes (IQR: 30.5-41.8 minutes). The median amount of bicarbonate injection was 100.2 mEq (IQR: 66.8-104.4). Patients who received a sodium bicarbonate injection during prolonged CPR had a higher percentage of return of spontaneous circulation, but not statistical significant (ROSC, 40.0% vs. 32.3%; P = .465). Sustained ROSC was achieved by 2 (6.7%) patients in the sodium bicarbonate treatment group, with no survival to discharge. No significant differences in vital signs after ROSC were detected between the 2 groups (heart rate, P = .124; systolic blood pressure, P = .094). Sodium bicarbonate injection during prolonged CPR was not associated with ROSC after adjust for variables by regression analysis (Table 3; P = .615; odds ratio, 1.270; 95% confidence interval: 0.501-3.219)
Conclusions
The administration of sodium bicarbonate during prolonged CPR did not significantly improve the rate of ROSC in out-of-hospital cardiac arrest.
IAH and ACS are under appreciated. They occur in a variety of medical and surgical critical illnesses. Diagnosis is easy once you think of it. Vigilance is required. The topic was recently reviewed here. Previous blog posts here, here and here.
Why do we need oxygen? Why does cyanide kill?
We've long known that patients are at increased risk early following hospital discharge---for the first 30 days or so. What is less well appreciated is that only about a third of early readmissions are for the same diagnosis as the original admission. Rather, there appears to be a general state of vulnerability and poor reserve early after hospitalization irrespective of the original diagnosis. Hence the notion of post-hospital syndrome. Free access to the perspective piece and audio interview here.
But not ready for prime time. The topic was recently reviewed. From the opening section of the review:
The increased need for MRI in PPM patients has prompted the development of a specifically designed pacemaker and lead system tested for safe use in the MRI environment and in early 2011, the US Food and Drug Administration (FDA) approved the first cardiac pacemaker designed to be used safely but conditionally during MRI examinations.[7]
Historically the hazards of MRI in pacemaker patients have included inhibition, “throwing the reed switch” leading to asynchronous pacing, reprogramming, current induction in the lead causing thermal injury at the tip and even myocardial perforation. And more.
All the manufacturers are working on MRI compatible devices and the field is evolving rapidly.
With emphasis on newer models and the modes available.
From a recent paper in JAMA Internal Medicine:
Methods To determine whether preoperative hyponatremia is a predictor of 30-day perioperative morbidity and mortality, we conducted a cohort study using the American College of Surgeons National Surgical Quality Improvement Program database...
Results..Preoperative hyponatremia was associated with a higher risk of 30-day mortality (5.2% vs 1.3%; adjusted odds ratio [aOR], 1.44; 95% CI, 1.38-1.50), and this finding was consistent in all the subgroups. This association was particularly marked in patients undergoing nonemergency surgery (aOR, 1.59; 95% CI, 1.50-1.69; P less than .001 for interaction) and American Society of Anesthesiologists class 1 and 2 patients (aOR, 1.93; 95% CI, 1.57-2.36; P less than .001 for interaction). Furthermore, hyponatremia was associated with a greater risk of perioperative major coronary events (1.8% vs 0.7%; aOR, 1.21; 95% CI, 1.14-1.29), wound infections (7.4% vs 4.6%; 1.24; 1.20-1.28), and pneumonia (3.7% vs 1.5%; 1.17; 1.12-1.22) and prolonged median lengths of stay by approximately 1 day.
Hyponatremia seems to be a marker of frailty. There is no evidence here that correction of hyponatremia would reduce these complications.
High quality does not mean lower cost. In fact the relationship is all over the map in this analysis.
Well, the idea seems to be that character and other intangible attributes of applicants are important and not just academic performance according to this NEJM piece. It's true, of course, although it's nothing new. It's what admissions committees have been after for decades and has long been the focus of applicant interviews and letters of recommendation. But in the minds of some these matters are getting more attention which is refreshing given our rising obsession with measurement in medical education.
In the audio segment accompanying the article the discussant points to a common fallacy in discussions of this topic: the false dichotomy between academic prowess in the sciences and the humanistic qualities desirable in a physician.
A few months ago marked the twentieth anniversary of the launch of evidence based medicine (EBM). Now seems a good time for a retrospective. After twenty years what does EBM mean? Where has it taken us? What are the distortions and unintended consequences? You might be surprised.
What I intend to do is start with a little of the history of EBM, talk about the essential notion as originally conceived by the founders, and mention a little about the process as applied to clinical practice today. Then I'll deal with some distortions and misconceptions as well as some surprising unintended consequences.
EBM was launched on November 4 1992 with the publication of this paper in JAMA. I don't recall noticing the paper coming out but when discussions of EBM as a new movement became popular I wondered what was so new about it. After all I thought I had always made clinical decisions based on evidence. I recalled so many of the clinical trials I had applied in my practice through the years. Practicing doctors for the most part, I thought, were conscientious in applying this evidence to their clinical decisions.
What I later learned was that it was not the reliance on evidence but the manner in which it was applied that was new. EBM sought to take things to a new level with a more systematic and rigorous approach to the application of research data.
Very soon after the publication of the JAMA paper, however, misconceptions began to fly. These mainly centered around the idea that EBM was “one size fits all” or “cookie cutter” medicine. That distortion persists today. More on that below. But it prompted some of the founders to publish another paper, which I regard as the second founding document, a paper in BMJ titled Evidence based medicine: what it is and what it is and what it isn't. In it we find what is most widely quoted today among aficionados as the essential definition:
It's about integrating individual clinical expertise and the best external evidence...
Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients.
Note that EBM is about individual expertise and judgment and about the individual patient. More on that below.
What about the process? It's useful to take a look at that because it can be rather onerous and I suspect that not many of us today practice it in its pure form chiefly because of the time it takes. I covered the process of EBM in a couple of long posts a few years ago. Suffice it to say here that it starts with asking a clinical question focused on your patient and converting it into a set of search terms that can be applied to a search engine such as PubMed. Citations thus retrieved are appraised according to a set of criteria after the model of the EBM pyramid. There are several variations on the basic pyramid theme, an example of which is shown here. Using the criteria the list of citations is trimmed down to those articles that are current and deemed of sufficient quality. The final step involves taking the information thus selected and applying it to the patient's idiosyncrasies including circumstances, preferences and values.
That last piece is often lost in discussions today when EBM is invoked to guide public policy. Herein lies one of the more pervasive distortions of EBM. Public policy discussions about the direction of health care got into high gear early in the Obama administration when the gimmicky phrase “comparative effectiveness research” entered the lexicon and debates raged about health care reform. There were diverse arguments about the direction health care should go but many of them sought to homogenize it, citing such things as the Dartmouth Atlas data and other sources which showed variation in delivery. The idea was that through various forms of central control one could minimize the variation which after all many believed to be the enemy of quality and efficiency. Pathways, performance measures, positive incentives and negative incentives all seek to do this and many proponents try to bolster their arguments by appealing to EBM. They thereby only reflect their ignorance about what EBM is. Maybe you like central control and can make some good arguments for it but you can't invoke EBM to support those arguments. EBM is diametrically opposed to central control. If you've any doubt about whether EBM concerns primarily individual decision makers and individual patients, watch this interview with David Sackett, one of the movement's founders:
I don't purpose to argue against central control here. Maybe it has something to recommend it but by definition the more external forces encroach on your decision making the less you will practice EBM. Just by definition.
But even when EBM is practiced according to its core principles there are unintended consequences. These relate to a fatal flaw of EBM found in that pyramid I referenced earlier. What I am referring to is that though not intended by its founders, application of EBM has led to numerous promotions of quackery. I have cited examples of this many times before as have David Gorski and other bloggers. It has to do with placing scientific plausibility at the bottom of the EBM pyramid, as I once explained:
...that this failure of EBM is more than just one of occasional unintended consequences. While it may have been unintended in the minds of the original founders, now it's systematic.
The problem is illustrated by the evidence pyramids, which are at the very core of the teaching about EBM. There are numerous versions of these pyramids, and Gorski links to a few examples, but what they have in common is that they put biologic plausibility (variously termed basic science, physiologic rationale, etc) at the bottom if they include it at all.
A casual observer might think that putting basic scientific rationale at the bottom means it's intended to be foundational (remember the old stepped care diagrams for treatment of hypertension and rheumatoid arthritis?). But that's not the way the EBM hierarchies of evidence are designed. Instead, higher levels on the pyramid trump those below. Students of EBM are taught to start at the top of the pyramid and “drill down,” level-by-level, until they find the evidence they want, and stop there.
Kimbal Atwood had a good example of how this has been applied to promote nutty ideas like homeopathy, in which occasional weak clinical trials which appear to favor homeopathy by chance variation trump overwhelming basic science information against it:
When this sort of evidence is weighed against the equivocal clinical trial literature, it is abundantly clear that homeopathic “remedies” have no specific, biological effects. Yet EBM relegates such evidence to “Level 5”: the lowest in the scheme. How persuasive is the evidence that EBM dismisses? The “infinitesimals” claim alone is the equivalent of a proposal for a perpetual motion machine. The same medical academics who call for more studies of homeopathy would be embarrassed, one hopes, to be found insisting upon “studies” of perpetual motion machines. Basic chemistry is still a prerequisite for medical school, as far as I’m aware.
The way we got into this fix is that the founders of EBM realized we couldn't rely only on scientific rationale. That has gotten us into trouble in the past. High level outcome based evidence is needed to be placed in the mix to address that problem. But what the EBM apologists left out was the fact that while scientific plausibility couldn't be the sole basis for making clinical decisions it couldn't be ignored. It needed to be a prerequisite.
Solutions? A group of physicians and scientists have recognized that EBM's unintended consequence could be avoided by giving basic scientific plausibility its due place while following the other EBM principles. You can find out lots more about that at their website.
So what do you think about EBM 20 years later? The verdict is mixed but it hasn't lived up to its promise. Maybe with the help of science based medicine (SBM) we'll get there.
In the May 17 2012 issue of the NEJM Ray et al reported an increased risk of sudden cardiac death attributable to the use of azithromycin. I blogged that issue here. The study was limited, being a cohort study based on administrative data and the absolute risk was low but its findings were compelling, particularly in regard to the timing of SCD in relation to the use of azithromycin. A more recent paper in the Journal failed to uphold the association of cardiac risk with azithromycin. A perspective piece in the same issue addresses the discrepancy between these studies. According to their analysis the findings of Ray et al are real and the discrepancy between the two studies may be attributable to differing patient populations and in the more recent paper a survival advantage attributable to azithromycin in the treatment of pneumonia that may have counterbalanced any adverse cardiac effect. It has long been known, of course, that macrolides as a class prolong the QT interval. Although that problem may not extend equally across the class there is plausibility to a risk of sudden cardiac death attributable to azithromycin.
They also point out findings in the Ray paper suggesting that levofloxacin has similar cardiac risk to azithromycin but not ciprofloxacin. Quinolones have been implicated in QT interval prolongation and Torsades but the risk appears not to extend equally across the class.
So what are we to make of all this? There are several points worth noting:
In the perspective piece the authors point out the FDA's statement regarding azithromycin:
On the basis of its review, the FDA approved revisions to azithromycin product labels regarding risks of QT-interval prolongation and the associated ventricular arrhythmia torsades de pointes. The revised labels advise against using azithromycin in patients with known risk factors such as QT-interval prolongation, hypokalemia, hypomagnesemia, bradycardia, or use of certain antiarrhythmic agents, including class IA (e.g., quinidine and procainamide) and class III (e.g., dofetilide, amiodarone, and sotalol) — drugs that can prolong the QT interval.
I would submit that those concerns would apply to the use of all macrolides as well as all quinolones with the possible exception of ciprofloxacin. That makes them somewhat impractical to implement but there are precautions that can be taken, in terms of minimizing the other risk factors I note below.
While the absolute risk of antibiotic induced QT prolongation and Torsades is low it is magnified by other risk factors that may interact and conspire to produce a catastrophic event. Hospitalization is a likely setting for the perfect storm that may bring these factors together. Hypomagnesemia and hypokalemia, both of which are powerful risk factors for QT prolongation, are common in hospitalized patients. Administration of proton pump inhibitors as “GI prophylaxis” to patients with pneumonia or other acute respiratory conditions causes hypomagnesemia. Poor oral intake, the common use of diuretics in the hospital and the use of normal saline as the default IV fluid may all produce hypokalemia. The concomitant use of other drugs known to prolong the QT interval (eg haloperidol and ondansetron) is common in hospitalized patients. So just being hospitalized may invite a combination of risk factors.
Recall as I pointed out year before last that patients who die while hospitalized with pneumonia tend to do so suddenly rather than according to any expected trajectory of hypoxia or organ failure. That observation just heightens the concerns mentioned above.
Finally, all that's new about this issue is the hype. The concerns have existed for a long time and over five years ago I cited a paper making the case that close attention to the electrocardiogram was warranted for any patient being treated for infection (or beyond that for most all patients sick enough to be hospitalized).
This is from the JAMA series on information for patients and families and is a nice easy to read summary of what they can expect as they navigate through the transition process.
As pointed out in this review, the classic form is a pediatric entity. When cases arise in adults they are less typical and the distinction from TTP is blurred. These cases are probably best termed TTP-HUS and should not argue against plasma exchange therapy.
Often in my professional development I am taught to consider the source. Information presented by pharmaceutical companies is to be rejected. Blogs are to be read with an extra measure of caution. A journal's reputation means something. Not so much anymore. Now we have to evaluate medical claims on their own merits regardless of the source. That demands a little more effort. Why do I say this? A case in point is the trend over the last few years in so called top tier medical journals toward the promotion of quackery. Just recently the Annals of Internal Medicine published this study on acupuncture for treatment of seasonal allergic rhinitis. The paper is cosmetically scientific with all the jargon and trappings of evidence based medicine:
Results: Compared with sham acupuncture and with RM, acupuncture was associated with improvement in RQLQ score (sham vs. acupuncture mean difference, 0.5 point [97.5% CI, 0.2 to 0.8 point; P less than 0.001]; RM vs. acupuncture mean difference, 0.7 point [97.5% CI, 0.4 to 1.0 point; P less than 0.001]) and RMS (sham vs. acupuncture mean difference, 1.1 points [97.5% CI, 0.4 to 1.9 points; P less than 0.001]; RM vs. acupuncture mean difference, 1.5 points [97.5% CI, 0.8 to 2.2 points; P less than 0.001]). There were no differences after 16 weeks in the first year. After the 8-week follow-up phase in the second year, small improvements favoring real acupuncture over the sham procedure were noted (RQLQ mean difference, 0.3 point [95% CI, 0.03 to 0.6 point; P = 0.032]; RMS mean difference, 1.0 point [95% CI, 0.2 to 1.9 points; P = 0.018]).
Limitation: The study was not powered to detect rare adverse events, and the RQLQ and RMS values were low at baseline.
Conclusion: Acupuncture led to statistically significant improvements in disease-specific quality of life and antihistamine use measures after 8 weeks of treatment compared with sham acupuncture and with RM alone, but the improvements may not be clinically significant.
Initially I just glanced casually at the study. This type of thing is not so unusual anymore. It was just another promotion of a nutty idea by a mainstream medical journal under the guise of evidence based medicine. It was so dense with scientific verbiage and so circumspect sounding I knew it would take a little effort to expose it. And at the time I was busy. And tired.
Well, fortunately Mark Crislip over at Science Based Medicine did it for me. When you read his post I suggest you skip down to the middle where he begins the actual analysis of the paper. The real devil is in the details and he unpacks them nicely:
The big difference is that acupuncture is a form of magic that is likely to get published in formerly reliable journals complete with positive spin: Acupuncture in Patients With Seasonal Allergic Rhinitis. A Randomized Trial...
A careful and critical reading of the paper gives compelling evidence that acupuncture does nothing, in line with all the other well-designed acupuncture studies. The cognitive disconnect between the editorial and conclusion and the data presented in the paper is a wonder to behold. And most people will read only the spin in the abstract and the editorial, not noticing the fatal flaws, and erroneously conclude that acupuncture has efficacy.
Yet another reason why I am glad I let my Annals subscription lapse years ago.
It's all quite ridiculous. One of the more unintentionally funny papers in the medical literature. Or was it intentional? It's hard to know from just reading the paper whether or not it's a parody. But apparently it was intended to be taken seriously because in an accompanying editorial the journal elevates it to the realm of public policy, specifically “comparative effectiveness research.”
This type of nonsense has been going on in high impact medical journals for several years now and it is getting worse. It started out in BMJ about a decade ago and over time has metastasized to other journals. Over at Quackwatch Steve Barrett put BMJ on his black list years ago and subsequently added the Annals.
But the Annals and BMJ have managed to maintain a good reputation, so now a journal's reputation means little. Whether it's indexed in Medline means little. The same can be said of broad categories such as journals and blogs. It's strictly buyer beware. I've said for a long time that relying on the source to evaluate the quality of information is intellectually lazy. Now, as illustrated by the paper and editorial in question, it's flat out unreliable.
There's not much being done to stop the trend but as time and energy permit I'll do what I can to expose it. In the meantime maybe there's a positive here. It means, more than ever before, that we have to evaluate medical information on its own merits rather than considering too strongly the source. Something we should have been doing all along.
Not warranted in critically ill patients requiring volume resuscitation according to new JAMA meta-analysis.
According to this Mayo Clinic Proceedings review:
Milk-alkali syndrome (MAS) consists of hypercalcemia, various degrees of renal failure, and metabolic alkalosis as a result of ingestion of large amounts of calcium and absorbable alkali. This syndrome was discovered in the 1930s after treatment of peptic ulcer disease with milk and sodium bicarbonate had become common.1 Initially considered a rare condition, MAS is now believed to be the third most common cause of in-hospital hypercalcemia, after hyperparathyroidism and malignant neoplasms.2
Nowadays it might better be named calcium-alkali syndrome. The old culprits, milk and baking soda, once used to treat peptic ulcer, have been replaced by calcium carbonate antacids. Re-emergence of the syndrome is due to increasing popular awareness of the problem of osteoporosis.
Another review was published more recently. I should point out an error in that review. Calcitriol is mentioned as an adjunctive treatment. I think they meant to say calcitonin.
Patient centered decision making is a core principle of evidence based medicine (EBM). A recent Annals paper looked at patient centered decision making and demonstrated a positive effect on outcomes:
Background: Patient-centered decision making (PCDM) is the process of identifying clinically relevant, patient-specific circumstances and behaviors to formulate a contextually appropriate care plan.
Medicine by central control as is being pushed by many today cannot accommodate patient-specific factors and is thus in conflict with patient-centered decision making and EBM.
More from the article:
Objective: To ascertain whether encounters in which PCDM occurs are followed by improved health care outcomes compared with encounters where there is inattention to patient context.
Design: Patients surreptitiously audio-recorded encounters with their physicians. Medical records of these encounters were then screened for “contextual red flags,” such as deteriorating self-management of a chronic condition, that could reflect such underlying contextual factors as competing responsibilities or loss of social support. When a contextual factor was identified, either as a result of physician questioning or because a patient volunteered information, physicians were scored on the basis of whether they adapted the care plan to it...
Results: Among 548 contextual red flags, 208 contextual factors were confirmed, either when physicians probed or patients volunteered information. Physician attention to contextual factors (both probing for them and addressing them in care plans) varied according to the presenting contextual red flags. Outcome data were available for 157 contextual factors, of which PCDM was found to address 96. Of these, health care outcomes improved in 68 (71%), compared with 28 (46%) of the 61 that were not addressed by PCDM (P = 0.002).
Here's a nice review from CCJM.
A review was recently published in the Annals of Internal Medicine.
It's difficult to parse because it only cites other reviews and policy documents, not primary sources. It lists ten measures “strongly encouraged” and twelve “encouraged” for “adoption now.”
The strongly encouraged measures are:
1) Pre-op and anesthesia checklists
2) Central line checklists and other bundles
3) Process interventions to reduce urinary catheter use (reminders, etc.)
4) VAP bundles
5) Hand cleaning
6) Do not use abbreviation lists
7) Interventions to reduce pressure ulcers
8) Barrier precautions
9) Ultrasound guidance for central line placement
10) Interventions to increase VTE prophylaxis
Items 1 and 2 have good evidence to support them. Anesthesia should be singled out as a remarkable success story but that effort was started decades ago and predates what we think of today as the patient safety movement. And it was done quietly, without the hype and public policy intrusions that characterize today's effort.
Interventions to reduce urinary catheter use (item 3) seem reasonable even if not evidence based. I have not formally reviewed the topic but have followed it closely and am aware of no strong research evidence that such interventions actually improve outcomes. Things are going in the right direction, though (somebody must be doing something right) based on a study I cited over a year ago demonstrating a decline in catheter related UTI. The trend cannot be attributed to Medicare's “no pay for errors” initiative concerning catheters, however, because it long predated the policy.
The evidence has been mixed concerning item 4 (VAP bundles). We are on a learning curve as to which components are most effective.
Item 5, hand washing, has been recognized as beneficial for over a century. Efforts to improve adherence are laudable. Giving it the status of a reportable measure, however, may distract from other equally if not more important infection control measures. The stethoscope, for example, of little clinical use today due to vanishing operator skill, remains in heavy use as a CPT coding instrument and is arguably as important as the hands in spreading infection (one in three stethoscopes carry MRSA).
I won't go over the rest of the top ten point by point. All are good ideas but suffer from lack of supporting evidence and/or the unintended consequences of turning them into reportable measures. Most have already been widely adopted for years if not decades.
Put mildly, items 11-22 are a little more interesting:
11) Multicomponent interventions to reduce falls
12) Use of clinical pharmacists to reduce adverse drug events
13) Documentation of patient preferences for life sustaining treatments
14) Obtaining informed consent for procedures
15) Team training
16) Medication reconciliation
17) Practices to reduce radiation exposure
18) The use of surgical outcome measures and report cards
19) Rapid response systems
20) Use of complementary methods to detect adverse events and medical errors
21) Computerized physician order entry
22) Simulation exercises
My head swims. OK, let's go through it.
11 and 12....check. We've been doing them for years.
13....pretty much implemented by law in 1990 and a nearly universal practice for many years.
14, 15....not exactly new ideas
16....med rec? Hmmm. Seems I recall that becoming a Joint Commission standard seven years ago. A wonderful idea in the abstract but a failure in the real world. Not that we shouldn't keep trying, but it's been a failure.
17....OK, why not?
18....Evidence in support of public reporting has been mixed but largely negative. It's loaded with unintended consequences.
19....Evidence for benefit from rapid response systems weighs slightly in favor of them but it is fairly weak. Almost all hospitals already have them due to Joint Commission's standard for systems to summon help for deteriorating patients.
20....OK
21....Ahh yes. CPOE. Almost all the research in support of it involves artificial surrogates. There is little if any evidence that it improves meaningful clinical outcomes. There is some evidence that it may be harmful early after adoption. In essence CPOE adds secretarial duties to the doctor's work flow thus replacing the unit secretary. Proponents argue that it eliminates a processing step thereby eliminating an opportunity for error. It is equally plausible that the eliminated step (the unit secretary) is a layer of safety and that the secretarial duties distract the doctor from clinical decision making. Well, whatever one's belief about benefit versus harm it's a moot point because we are well on our way to universal adoption. If experience with CPOE has taught us anything it's that haste magnifies the unintended consequences, so to use it for all it's worth and avoid harm we must go slow in development, training and implementation. That's why I am uncomfortable with any pressure for “adoption now” as a safety measure.
22....Simulation exercises? Sounds like a great idea. Resource intensive though. Where's the evidence?
Aside from the problem that much of the above lacks evidential support, there are no new ideas presented. Most of the measures, evidence based or not, have been widely adopted for some time. So I would find these recommendations to be of little help in advancing the cause of patient safety. But the paper does shed light on why the patient safety movement has failed to live up to its promise. The Consumers Union declared the patient safety movement a failure a decade after the IOM report which many credit with the start of the movement. More recently Bob Wachter, one of the authors of the Annals paper and an ardent systems guy to boot worried that the patient safety movement is in danger of flickering out. He cites physician burnout as one of the reasons.
So why in the world would physicians burn out on patient safety? I think it's because doctors want tools, not rules. They recognize that rules as promulgated by today's systems approaches to patient safety, being onerous and loaded with unintended consequences, should be supported by good evidence. But they're not, for the most part. And as important as systems of care are (yes, I do believe we need a systems approach to patient safety) doctors all too often see them as substitutes for thought and judgment.
Speaking of unintended consequences I'll conclude with one that deserves special mention. When the Institute of Medicine launched the patient safety movement its intention was to de-emphasize blame (as implied in the title of its report To Err is Human) in order to create a culture of transparency and facilitate reporting and analysis of adverse outcomes. But the IOM got carried away in its zeal and egregiously hyped the data on medical harm by equating it to a jumbo jet crashing daily. Even worse than hyping, the IOM actually misrepresented the study on which it based its claims, prompting a lead author of the original report to issue, in the New England Journal of Medicine, a criticism of their spin. A retraction of sorts. But it received little notice and the IOM hype took on a life of its own leading to a heightened culture of blame concerning patient safety, the opposite effect to what was originally intended. I've detailed the whole mess here and other places.
From a recent paper in JAMA Internal Medicine:
Methods Patients received enoxaparin sodium, 1 mg/kg, every 12 hours or 1.5 mg/kg once daily between June 1 and November 30, 2009. Moderate renal impairment was defined as creatinine clearance (CrCl) of 30 to 50 mL/min. Normal renal function was defined as CrCl greater than 80 mL/min. The primary outcome was major bleeding, defined as any bleeding resulting in death, hospital admission, lengthened hospital stay, or an emergency department visit. The secondary outcome was thromboembolism.
Results A total of 164 patients met the inclusion criteria: 105 with normal renal function and 59 with moderate renal impairment. The primary outcome occurred in 6 of 105 patients (5.7%) with normal renal function vs 13 of 59 patients (22.0%) with moderate renal impairment, representing an unadjusted odds ratio of 4.7 (95% CI, 1.7-13.0; P = .002).
That's rather concerning. FDA approved labeling calls for no adjustment until the clearance is below 30 ml/min. So the patients in the reduced renal function group all received the drug “appropriately” according to the approved labeling. Alternatives to address this situation might include the use of unfractionated heparin or enoxaparin dose adjustment based on antiXa monitoring.
From a recent meta-analysis:
In a pooled analysis of data of 31 RCTs measuring the effect of CCBs on stroke, CCBs reduced stroke more than placebo and β-adrenergic blockers, but were not different than ACEIs and diuretics. More head to head RCTs are warranted.
Quite often one encounters a wide QRS in the dominant rhythm of the electrocardiogram which may have features of either or both bundle branch blocks but is typical of neither. It is often referred to as nonspecific intraventricular conduction delay (IVCD). If the condition is chronic and stable (that is, not due to external factors such as drug effects or hyperkalemia) it generally represents diffuse myocardial scarring and it's a sure bet the patient's ejection fraction will be reduced.
One such pattern, recently described in this paper which caught my eye, is characterized by the RBBB pattern in the precordial leads but with the LBBB pattern in the limb leads and has been termed masquerading BBB. It has been conceptualized in various ways but represents bilateral conduction system disease as a reflection of multifocal myocardial scarring, reflecting extensive damage. It tends to be a poor prognostic sign.
One of the early papers on this topic, back in the days of physician-scientists when autopsies were done and doctors were actually interested in clinicopathological correlations, is here and it is a fascinating read.
PICCs (or PICC lines to those suffering from the redundant acronym syndrome) have become popular because they offer a convenient option for IV access and blood sampling. They are becoming the default option for patients who are a “tough stick” or have special IV therapy needs. These are usually the sicker patients who are likely to have CKD. But there's a problem in CKD patients. PICC use may jeopardize future dialysis access and current guidelines discourage the practice.
But a recent study presented at the National Kidney Foundation meeting (via Medpage Today) showed that the practice is common in advanced CKD patients. According to one of the discussants:
She explained that at her institution, they have started a program to reduce PICC placement in CKD patients. "For anyone with a glomerular filtration rate of less than 30 mg/L, you cannot just order a PICC. You have to go through an algorithm where you consider other line placements."
Remove? Treat through? Antibiotic lock?
A practical review is presented here and the IDSA guidelines for IV catheter related infections in general are here.
From the paper:
Dural sinus or cerebral venous thrombosis (CVT) is a frequently unrecognized cause of stroke affecting predominantly young women. Typical clinical signs include headache, visual problems and seizures.
Fairly easy to diagnose and treat once you think of it.
An update. Free full text via Medscape.
Recent paper here in JAMA Internal Medicine. Variability may be driven by the paucity of high level data, variable resources at different hospitals and marked variations in current guidelines.
Perspective offered here in Medpage Today.
That's a popular concern but available evidence suggests it doesn't.
Pause for a little metacognition by reading these tips. None of them will do you any good, of course, if you don't have enough time to spend with patients.
Most are outflow tract tachycardias and most of those are right ventricular. They are unique in that while they tend to be benign they may cause tachycardia mediated DCM and are amenable to ablation. (They may respond to calcium blockers too but leave that to the experts). Also don't forget that right ventricular cardiomyopathy may manifest as RV tachycardia. This review focuses on RVOT.
It has been known for a while now that pneumonia is a short term risk factor for acute coronary syndrome. So it recently occurred to some investigators to see if adding an aspirin a day to the regimens of pneumonia patients would help. The results were startling:
..the rates of ACS at 1 month were 1.1% (n=1) in the aspirin group and 10.6% (n=10) in the control group (relative risk, 0.103; 95% confidence interval 0.005–0.746; P=0.015). Aspirin therapy was associated with a 9% absolute reduction in the risk for ACS. There was no significant decrease in the risk of death from any cause (P=0.151), but the aspirin group had a decreased risk of cardiovascular death (risk reduction: 0.04, P=0.044).
New review here (free full text provided by Medscape).
Points of interest:
Budd–Chiari syndrome is a rare disorder caused by hepatic venous outflow obstruction and resulting hepatic dysfunction....
BCS is defined as hepatic venous outflow obstruction at any level from the small hepatic veins (HV) to the junction of the IVC and the right atrium, regardless of the cause of obstruction. Outflow obstruction caused by the sinusoidal obstruction syndrome (formerly 'veno-occlusive disease') and cardiac disorders is excluded...
Hepatic venous outflow obstruction caused by external compression or invasion of the venous lumen is termed secondary BCS and is seen with malignant tumors or large cysts...
B-C can be considered a disease of thrombophilia:
At least one thrombophilic disorder is identifiable in 84% of patients and multiple disorders are found in 46%...
Myeloproliferative disorders (MPD) deserve specific mention due to their high frequency in BCS. MPD result in excess cell production by the bone marrow and include: chronic myeloid leukemia, primary myelofibrosis, polycythema rubra vera and essential thrombocytosis. These disorders are particularly common in patients with BCS and may be overt or occult (occurring with normal peripheral blood counts). MPD is found in 49% of BCS cases who undergo a bone marrow examination.
The importance of JAK 2:
In the setting of BCS or splanchnic thrombosis, the positive predictive value rises further and JAK2 (V617F) mutation is a very reliable marker for MPD. A recent meta-analysis of 23 studies reported a pooled prevalence of 37 and 24% of patients with BCS and portal vein thrombosis respectively.
That said, virtually all the other thrombophilias have been associated with B-C.
The clinical presentation can be acute (with abdominal pain) or chronic, and range from asymptomatic to acute liver failure and include encephalopathy, variceal bleeding and splenomegaly.
In addition to treatment of any underlying diseases and general supportive management of the liver disease anticoagulation, shunting, vascular stenting and transplant are discussed as treatment options. There is very limited experience with thrombolysis.
