Here is a case report and concise review.
From the paper:
Boerhaave's syndrome is readily suspected in a patient with a history of overindulgence in food or drinks who, after severe or repeated vomiting, experiences excruciating chest pain and develops subcutaneous emphysema [3]. However, up to one-third of patients have atypical symptoms or are admitted with severe respiratory distress and/or shock. The differential diagnosis of Boerhaave's syndrome includes a variety of acute thoracic and abdominal conditions including myocardial infarction, pulmonary embolus, dissecting aorta, ruptured aortic aneurysm, perforated peptic ulcer, Mallory-Weiss syndrome, pancreatitis, pneumonia, and spontaneous pneumothorax [4].
Traditionally the electrocardiographic early repolarization pattern has been considered benign. The last decade, however, has raised awareness of a subset of patients with this pattern who are at risk for sudden cardiac death. With advances in our understanding this subset has emerged as a new channelopathy. Distinguishing characteristics which differentiate the malignant variety (now termed early repolarization syndrome, ERS) from benign early repolarization (which is fairly common in the general population) are now better defined. This free full text review summarizes the latest evidence, provides some illustrative tracings and discusses an algorithm for evaluation.
The distinction can be difficult even when the accepted ARVD criteria are applied. Based on the Hopkins experience there are some clues though:
Conclusions—The 2010 diagnostic criteria for ARVD/C have limited discrimination in distinguishing between ARVD/C and CS. Despite the overlay in clinical presentation, older age of symptom onset, presence of cardiovascular comorbidities, nonfamilial pattern of disease, PR interval prolongation, high-grade atrioventricular block, significant left ventricular dysfunction, myocardial delayed enhancement of the septum, and mediastinal lymphadenopathy should raise the suspicion for CS.
The conclusion from recent findings:
Even at the highest performing hospital, discharge summary quality is insufficient in terms of timeliness, transmission, and content. Improvements in all aspects of discharge summary quality are necessary to enable the discharge summary to serve as an effective transitional care tool.
Elements that were missing in almost all discharge summaries were discharge weight and discharge volume status. Discharging patients “too wet” has previously been cited as a driver of recurrent heart failure hospitalizations.
This is a diagnosis you want to make early. Here's a very helpful review.
A post at Academic Life in Emergency Medicine, which cites the review, has a lot of pearls. It notes this regarding the medicolegal risk:
About 84% of the plaintiff verdicts involved a situation where the patient experienced permanent bowel or bladder dysfunction. Plaintiffs were more likely to win in cases when deficits developed after presentation, specifically when CES was initially missed. When patients present with incontinence, the plaintiff only won 16% of the cases [2].
Hence the importance of carefully documenting the patient's findings on initial presentation.
In this series of patients seen at the Mayo Clinic in Arizona several points are noteworthy:
It accounts for 15%–29% of community-acquired pneumonia in Arizona.
Symptom and radiographic resolution is slow, a matter of weeks.
It has seen a dramatic increase in Arizona. From the article:
The incidence of infection in this coccidioidomycosis-endemic area has considerably increased from 5.3 cases per 100,000 population in 1998 to 42.6 cases per 100,000 population in 2011.
Treatment criteria are controversial. Again, from the article:
Although the Infectious Diseases Society of America treatment guidelines acknowledge differences of expert opinion regarding the need to treat primary coccidioidomycosis (23), the guidelines suggest identifying characteristics to facilitate diagnosis of moderate to severe infection in patients who might benefit from treatment (23). These guidelines recommend possible antifungal treatment for patients with symptoms lasting greater than 2 months, night sweats greater than 3 weeks, weight loss of greater than 10%, inability to work, serologic complement fixation titer greater than 1:16, bilateral infiltrates or involvement of at least one half of 1 lung, or prominent or persistent hilar adenopathy (23).
The field is moving ahead but not ready for prime time. This review is one of the better ones I've seen on the topic. Free full text.
Yes, the same Richard Baron who just two months later sent out the “We're sorry. We got it wrong” email to ABIM diplomats. You can watch the debate here. I was not aware of this video until just the other day, following ABIM's announcement, from some of the comments on social media. It gave me a better understanding of what's going on and dampened my initial optimism about ABIM's February 3 announcement. Dr. Cutler's description of how our money is being spent by the board was shocking.
What was of particular interest to me was Dr. Baron's vigorous defense of MOC including the changes that went into effect in 2014. He claimed to have years of demonstrated need and evidential support to back up the changes. There was nothing tentative or circumspect in his arguments. He came across as one who had firmly made up his mind. How then do you get from there to “we got it wrong” in just two months? My skepticism concerning the February 3 announcement is heightened.
From a recent review:
Coronary subclavian steal syndrome (CSSS) is the reversal of blood flow in an internal mammary artery bypass graft that results in coronary ischemia. CSSS is an uncommon but treatable cause of coronary ischemia. In this review, we highlight the historical background and epidemiology of CSSS, common clinical presentations, diagnosis of CSSS and management strategies for relieving ischemia…
Recent findings: Most commonly, CSSS results from atherosclerotic stenosis of the subclavian artery and occurs in 2.5–4.5% of patients referred for coronary artery bypass grafting (CABG). All patients referred for CABG should have bilateral noninvasive brachial blood pressures checked to screen for the underlying subclavian stenosis. A review of 98 case reports with 128 patients demonstrated a diverse clinical presentation of CSSS, including acute myocardial infarction, unstable angina and acute systolic heart failure. Resolution of CSSS symptoms has been reported with both surgical and percutaneous revascularization. Long-term patency with either revascularization strategy is excellent. Percutaneous revascularization is largely considered the first-line therapy for CSSS and can be safely performed prior to CABG to prevent CSSS.
Summary: CSSS should be suspected in patients presenting with angina, heart failure or myocardial infarction after CABG. Successful amelioration of CSSS symptoms can be safely and effectively performed via percutaneous revascularization.
Ketoalkalosis?
That was the topic of this paper in the Southern Medical Journal. Diabetic ketoalkalosis (DKALK) refers to a complex acid base disorder in which diabetic ketoacidosis (DKA) coexists with a separate process causing metabolic alkalosis. This results in a rise in the delta ratio (DR, or delta gap/delta bicarb) to greater than 1.2 when, in simple DKA it should be around 1.0. Put another way, the coexisting metabolic alkalosis prevents the bicarb from falling as much as would be expected from the rise in the anion gap. It's a misnomer, of course, because the ketosis does not cause the alkalosis; the alkalosis is a separate process. The alkalosis is believed due to vomiting and counter regulatory responses to volume loss. The DR could be incalculable if the metabolic alkalosis is severe enough that the bicarb (and pH) are normal.
Don't forget that the opposite can occur. A DR less than 0.8 suggests a second process causing metabolic acidosis such as lactic acidosis.
From a new study in JAMA:
Conclusions and Relevance Sustained, community-wide programs targeting cardiovascular risk factors and behavior changes to improve a Maine county’s population health were associated with reductions in hospitalization and mortality rates over 40 years, compared with the rest of the state. Further studies are needed to assess the generalizability of such programs to other US county populations, especially rural ones, and to other parts of the world.
More from Cardiobrief.
From a recent review:
Core tip: Diabetic patients develop a cardiomyopathy that is independent of vascular disease, and is thought to develop as a direct result of the prolonged hyperglycaemia. Animal models of diabetes can help us understand the cellular mechanisms that lead ultimately to contractile dysfunction of diabetic cardiomyopathy. The streptozotocin rat model of type 1 diabetes has slowed Ca2+ transients and twitch force kinetics, with reduced myofilament Ca2+ sensitivity. Myocytes are decreased in volume in diabetic hearts, with reduced and disrupted F-actin, and type 1 collagen is increased. Together, these changes all contribute to the reduced contractility of diabetic cardiomyopathy.
Nowadays, with rising antimicrobial resistance outpacing the antibiotic pipeline, we increasingly have to consider pulling old drugs off the shelf. What about chloramphenicol? From a recent systematic review and meta-analysis:
Results Sixty-six RCTs fulfilled the inclusion criteria, and these included 9711 patients. We found a higher mortality with chloramphenicol for respiratory tract infections [risk ratio (RR) 1.40, 95% CI 1.00–1.97] and meningitis (RR 1.27, 95% CI 1.00–1.60), both without heterogeneity. The point estimate was similar for enteric fever, without statistical significance. No statistically significant difference was found between chloramphenicol and other antibiotics regarding treatment failure, except for enteric fever (RR 1.46, 95% CI 1.07–2.00, without heterogeneity). This difference derived mainly from studies comparing chloramphenicol with fluoroquinolones (RR 1.85, 95% CI 1.07–3.2). There were no statistically significant differences between chloramphenicol and other antibiotics in terms of adverse events, including haematological events, except for anaemia, which occurred more frequently with chloramphenicol (RR 2.80, 95% CI 1.65–4.75, I2 = 0%), and gastrointestinal side effects, which were less frequent with chloramphenicol (RR 0.67, 95% CI 0.46–0.99, I2 = 0%). Many of the studies included were sponsored by pharmaceutical companies marketing the comparator drug to chloramphenicol, and this might have influenced the results.
Conclusions Chloramphenicol cannot be recommended as a first-line treatment for respiratory tract infections, meningitis or enteric fever as alternatives are probably more effective. Chloramphenicol is as safe as treatment alternatives for short antibiotic courses.
Historically, the safety concern with chloramphenicol has been its hematologic toxicity. This study mitigates that concern somewhat but also found that newer agents tend to be more effective for its old indications.
Via Hospital Medicine Virtual Journal Club.
---was associated with a worse prognosis in patients with systolic heart failure and a narrow QRS complex in this study.
From the Medical Letter via JAMA.
From the article:
In patients with mild illness caused by a susceptible strain of influenza, starting treatment with a neuraminidase inhibitor within 48 hours after the onset of illness can decrease the duration of fever and symptoms and may also reduce the risk of complications such as pneumonia.3 In hospitalized and critically ill patients, observational studies indicate that these drugs can decrease the risk of death when started soon after symptom onset; the results of some studies suggest that treatment within 4-5 days after symptoms appear may still have some benefit.4- 6 The usual duration of treatment with a neuraminidase inhibitor is 5 days, but a prolonged treatment course (eg, 10 days) is often used for critically ill or immunocompromised patients, in whom viral replication may be protracted.
It is increased, both in the long and the short term.
The American Board of Internal Medicine's February 3 announcement came during a very busy week in hospital medicine for me and I have just now had time to process it. There is a lot to unpack. The announcement, which contains an apology and an acknowledgment that they “got it wrong,” is a welcome development but it raises many questions. Below is my very preliminary take.
What is the immediate impact?
For me, two items are significant:
Effective immediately, ABIM is suspending the Practice Assessment, Patient Voice and Patient Safety requirements for at least two years.
That is a great relief for me as I trudge through. Now I can focus on the learning activity, which is the important part. I get points for MKSAP, which I love doing and would have done anyway.
Within the next six months, ABIM will change the language used to publicly report a diplomate's MOC status on its website from “meeting MOC requirements” to “participating in MOC.”
That is in response to the problem I addressed here:
So what am I talking about? Well, for the grandfathered internists who choose not to perform the “voluntary” recertification activities the Board is coming as close to de-certifying them as they can without actually taking the certification away and having to say “Sorry. We lied.”
How does it work? It's in the way they report your certification status. Go to their website and look up the name of a grandfathered colleague (this portion of the site is open to the public). Those not participating are designated as Certified but right under that it says Meeting Maintenance of Certification Requirements: No.
What will the public think? What will credentialing bodies think? While this will confuse some people it comes across loud and clear to most as nominally certified but not really certified.
While I am thankful they softened the language they have not fully addressed the problem, which is that in a round about way they went back on their promise of lifetime certification with voluntary maintenance.
ABIM's announcement is a positive step but is it enough?
For the practice assessment and patient safety modules, perhaps the most troublesome aspect of MOC, all they did was call a moratorium. Nobody knows what they will do with this in two years. These exercises were fundamentally flawed but ABIM did not acknowledge that. All they admitted was that they launched programs that weren't ready and that docs did not find meaningful. That leads to the question of what these programs will look like once ABIM deems them “ready.” What about the apology? Does it represent appeasement or is it genuine contrition? I will take a wait and see attitude. The move by ABIM was a first step but only that. Vigorous debate of the issues surrounding MOC needs to move forward.
Despite ABIM's pledge to freeze MOC fees the accusations of financial impropriety were not addressed.
These have been nicely summarized in a series of posts over at Dr. Wes. Whether the conflicts are real or only perceived they need to be addressed by the board in a manner that will restore the credibility of their leadership. I have yet to see movement in that direction.
Questions linger about CME.
In a recent post about the MOC discussion medical journalist Larry Husten said this:
As I said, CME can play a key role in MOC, but only when the doctors pay for it themselves. To start, every effort should be taken to remove industry’s role from CME.
In his thinking that would rule out most accredited category I offerings because, as he correctly implied in the same post, most of it is funded, to one degree or another, by industry.
A very vocal group of physicians agree with Mr. Husten. But if the ABIM leaders really mean what they said in the February 3 announcement it would appear that they disagree because they say that going forward they plan to recognize “most forms of ACCME-approved Continuing Medical Education.”
But one part of ABIM's statement on CME is concerning, from the FAQ page:
We are absolutely interested in finding ways to recognize meaningful clinical work that you do in your practices to earn CME points, and we're particularly interested in recognizing CME activities for which there is evidence that they drive learning and/or change practice. Many forms of “passive” CME do not meet this standard.
This implies that we're headed back to the practice improvement modules and, even worse, that the learning points may be tied to those activities. And what kind of evidential support are they looking for? I know of no robust evidence that ties any form of CME, inside or outside of MOC, to meaningful outcomes. We all know intuitively that knowledge helps drive better patient care but the idea that these processes with all their layers of complexity can be measured in a meaningful way strikes me as naive.
From a recent review:
Core tip: Hypertension is a major contributor to the development and progression of cardiovascular disease. Increased blood pressure often coexists with insulin resistance. The various antihypertensive drugs have different effect on glucose metabolism. Indeed, angiotensin receptor blockers as well as angiotensin converting enzyme inhibitors have been associated with beneficial effects on glucose homeostasis. Calcium channel blockers are considered to have neutral metabolic effects. On the other hand, diuretics and β-blockers have an overall disadvantageous effect on glucose metabolism. As a result the metabolic effects of the various blood pressure lowering drugs should be taken into account when selecting an antihypertensive treatment.
From a recent review:
The average survival is less than a year in untreated patients with severe cardiac impairment. However, if treated early and aggressively, the survival rate approaches that of the regular heart failure population.
This open access full text review examines the physiology and mechanism of dyspnea due to hyperinflation in COPD.
The cardiovascular effects of magnesium are multiple and complex. Here is a recent free full text review.
From the conclusion of the review:
Mg2+ has vasodilatory, anti-inflammatory, anti-ischemic, and antiarrhythmic properties (Fig. 3). It is a critically important nutrient and a potentially useful therapeutic agent in cardiovascular medicine. Several experimental, epidemiological, and clinical studies have established the role of Mg2+ in the pathogenesis of cardiovascular disorders. Currently, the use of Mg2+ is limited mostly for the prevention and/or treatment of cardiac arrhythmias. We believe that adequate Mg2+ intake should be a part of the heart healthy diet. However, there is a compelling need for several well-designed cohort studies to determine the interrelationship among dietary Mg2+ intake, serum (or intracellular) Mg2+ concentration, and CVD, and to provide concrete evidence on the risks and/or benefits of taking Mg2+ supplements. Future basic science research should be focused on gaining a better understanding of the metabolic effects of Mg2+ intake in health and disease. Lastly, larger well-designed, randomized controlled trials are needed to widen the therapeutic scope of this inexpensive nutrient.
From the Journal of Toxicology:
Objective. Limited reported data have reports effects after acute ingestion of methotrexate. Treatment recommendations do not differentiate between exposure routes. Our objective was to determine the frequency of significant toxicity effects and use of therapy after methotrexate ingestion in adults. Methods. We performed a retrospective study on adult cases reported to 6 poison centers over 6 years (2000–2005) which exceed 180,000 exposures/year.. No patient in the series received dialysis or died. The mean dose ingested for all patients was 24mg (range 2.5–100mg) and the mean dose for suicidal ingestions was 47.5mg (12.5–100mg). The most common clinical effects were abdominal pain, oral irritation, throat irritation, nausea, dizziness, and headache. Nine patients received folinic acid and 3 patients received sodium bicarbonate. No patient developed renal failure, bone marrow suppression, seizure, or coma. No patient died or received dialysis. Conclusion. In our series of patients from 6 poison centers over six years, 63 cases of acute adult methotrexate ingestions were reported. Methotrexate toxicity from ingestion in adults was uncommon and rarely toxic...
Methotrexate has been used in parenteral form as a chemotherapeutic agent for decades. In recent years, the oral form has been used for the treatment of rheumatologic conditions with both increased frequency and dosage [8]. Parenteral methotrexate toxicity has been examined, and several effects such as renal failure, respiratory failure, myelosuppression, and neurologic disruption have been described [1, 9]. Recent case reports have described fatal overdose of methotrexate ingestions, although no data from a large series of acute ingestions has been reviewed until now [4].
While several antidotes have been postulated for methotrexate toxicity, folinic acid (leucovorin) has been shown to be the most effective and has few known complications [10]. We found that the use of methotrexate-specific treatments was uncommon, possibly suggesting that physicians were unfamiliar with this rarely used drug or the physicians were not concerned the patients were ill and need it...
Based on these findings, supportive care and observational therapy without methotrexate-specific treatment should be considered in acute ingestions. Patients can be monitored for development of renal insufficiency, neurologic effects, or bone marrow suppression. Based on the clinical effects and followup, the measurements and reexaminations could be done as an inpatient or outpatient. A large, prospective study to evaluate this treatment approach is warranted.
From a recent review:
Obesity has become an important public health issue in Western and developing countries, with well known metabolic and cardiovascular complications. In the last decades, evidence have been growing about the active role of adipose tissue as an endocrine organ in determining these pathological consequences. As a consequence of the expansion of fat depots, in obese subjects, adipose tissue cells develope a phenotypic modification, which turns into a change of the secretory output. Adipocytokines produced by both adipocytes and adipose stromal cells are involved in the modulation of glucose and lipid handling, vascular biology and, moreover, participate to the systemic inflammatory response, which characterizes obesity and metabolic syndrome. This might represent an important pathophysiological link with atherosclerotic complications and cardiovascular events. A great number of adipocytokines have been described recently, linking inflammatory mileu and vascular pathology. The understanding of these pathways is crucial not only from a pathophysiological point of view, but also to a better cardiovascular disease risk stratification and to the identification of possible therapeutic targets.
This brief review discusses the consequences of pulmonary AV shunting. Free full text.
From a new paper in Stroke:
Background and Purpose—We examined blood pressure 1 year after stroke discharge and its association with treatment intensification...
Results—Among 3153 patients with ischemic stroke, 38% had greater than or equal to 1 elevated outpatient SBP eligible for treatment intensification in the 1 year after stroke. Thirty percent of patients had a discharge SBP less than or equal to 140 mm Hg, and an average 1.93 treatment opportunities and treatment intensification occurred in 58% of eligible visits. Forty-seven percent of patients discharged with SBP 141 to160 mm Hg had an average of 2.1 opportunities for intensification and treatment intensification occurred in 60% of visits. Sixty-three percent of the patients discharged with an SBP greater than 160 mm Hg had an average of 2.4 intensification opportunities, and treatment intensification occurred in 65% of visits.
Conclusions—Patients with discharge SBP greater than 160 mm Hg had numerous opportunities to improve hypertension control. Secondary stroke prevention efforts should focus on initiation and review of antihypertensives before acute stroke discharge; management of antihypertensives and titration; and patient medication adherence counseling.
I do have concerns with the authors' last suggestion that some patients' regimens need to be intensified while they are still in the hospital. It is common practice, and in accordance with the guidelines, to allow “permissive hypertension” in the early stages post ischemic stroke. Sometimes we even withhold patients' pre-admission antihypertensives. It is difficult at times to know just when to resume such medications let alone intensify a patient's regimen.
More from ACP Hospitalist Weekly.
This review from the green journal contains a lot of pearls applicable not only to the perioperative situation but to hospitalization in general. From the abstract:
Challenges in managing patients with Parkinson's disease in the perioperative hospital setting include disruption of medication schedules, “nothing by mouth” status, reduced mobility, and medication interactions and their side effects. Patients with Parkinson's disease are more prone to immobility and developing dysphagia, respiratory dysfunction, urinary retention, and psychiatric symptoms. These issues lead to higher rates of pneumonia, urinary tract infections, deconditioning, and falls compared with patients without Parkinson's disease, as well as prolonged hospital stays and a greater need for post-hospitalization rehabilitation. Steps can be taken to decrease these complications, including minimizing nothing by mouth status duration, using alternative routes of drugs administration when unable to give medications orally, avoiding drug interactions and medications that can worsen parkinsonism, assessing swallowing ability frequently, encouraging incentive spirometry, performing bladder scans, avoiding Foley catheters, and providing aggressive physical therapy. Knowing and anticipating these potential complications allow hospital physicians to mitigate nosocomial morbidity and shorten recovery times and hospital stays.
This is an interesting read and it is available as free full text.
Some of the features of the article:
Recent changes in the maintenance or certification (MOC) process are briefly reviewed.
A web based petition now has over 19000 anti-MOC signatures.
MOC is not supported by outcome based evidence, though some research has been done.
Claims that MOC has solid support from practicing physicians are debunked.
The relevance of MOC to the realities of clinical care is questioned.
The American Board of Internal Medicine is beset with the perception, if not the reality, of financial conflict of interest.
The MOC process has been criticized formally by numerous professional organizations, one of which has a lawsuit pending against the American Board of Medical Specialties.
The article concludes:
Regardless of how the MOC issue is resolved, the recent focus on the ABIM has shed a bright light on how medicine is regulated in the United States. The ABIM is a private, self-appointed certifying organization. Although it has made important contributions to patient care, it has also grown into a $55-million-per-year business, unfettered by competition, selling proprietary, copyrighted products. I believe we would all benefit if other organizations stepped up to compete with the ABIM, offering alternative certification options.
More broadly, many physicians are waking up to the fact that our profession is increasingly controlled by people not directly involved in patient care who have lost contact with the realities of day-to-day clinical practice. Perhaps it's time for practicing physicians to take back the leadership of medicine.
From a recent report in the Journal of the American Heart Association:
Methods and Results In France, serious cases of abuse and dependence in response to the use of psychoactive substances must be reported to the national system of the French Addictovigilance Network. We identified all spontaneous reports of cardiovascular complications related to cannabis use collected by the French Addictovigilance Network from 2006 to 2010. We described the clinical characteristics of these cases and their evolution: 1.8% of all cannabis‐related reports (35/1979) were cardiovascular complications, with patients being mostly men (85.7%) and of an average age of 34.3 years. There were 22 cardiac complications (20 acute coronary syndromes), 10 peripheral complications (lower limb or juvenile arteriopathies and Buerger‐like diseases), and 3 cerebral complications (acute cerebral angiopathy, transient cortical blindness, and spasm of cerebral artery). In 9 cases, the event led to patient death.
Conclusions Increased reporting of cardiovascular complications related to cannabis and their extreme seriousness (with a death rate of 25.6%) indicate cannabis as a possible risk factor for cardiovascular disease in young adults, in line with previous findings. Given that cannabis is perceived to be harmless by the general public and that legalization of its use is debated, data concerning its danger must be widely disseminated. Practitioners should be aware that cannabis may be a potential triggering factor for cardiovascular complications in young people.
The video below is a medical grand rounds presentation by Dr. Weed at Emory
in 1971.
Noteworthy:
There are several shots of J. Willis Hurst and Nanette Kass Wenger on the front row starting at 11:39. Following that presentation Hurst went on to champion the problem oriented medical record.
At 22:30 Weed points out that we should avoid jumping to a premature diagnosis by stating a problem only at the level of resolution we have at the time pending further data or expertise.
At 33:53 Weed states: “The problem list should not have 'rule outs', question marks or 'probables'; it should be a precise reproducible statement of the problem at the level you can undersstand it and guarantee it no matter how unsophisticated you have to get.”
Even with the problem lists embedded in today's EMR we're not nearly as rigorous in our approach as Weed envisioned 44 years ago.
Check out the transcript and audio here of an interview with one of MOC's main detractors who proposes alternative means for accountability which would be less burdensome, more clinically relevant and less expensive.
From a recent study of very young patients presenting with ACS:
Results
A total of 124 patients met inclusion criteria. The mean age was 31 ± 4 years for both sexes. Approximately half (49%) of the patients were obese (body mass index greater than or equal to 30 kg/m2); 90% of patients had at least 1 traditional risk factor, most commonly hyperlipidemia (63%) and smoking (60%); 52% of patients underwent re-vascularization, of which 94% were by percutaneous coronary intervention, and 42.9% of patients had intracoronary thrombus, of whom approximately one third had no detectable underlying coronary disease.
Conclusions
Very young patients with acute coronary syndrome tend to be obese, with a high prevalence of smoking and hyperlipidemia. The presence of thrombus in the absence of underlying coronary disease suggests a thromboembolic event or de novo thrombotic occlusion, which may reflect primary hemostatic dysfunction in a considerable number of these patients.
When I first saw the title of this paper I was expecting to see a lot of novel genetic risk factors, but apparently the investigators did not look for those.
Among the lessons in this case from Dr. Smith's ECG blog:
Acute proximal coronary occlusion may present with ST depression as the principal ST segment abnormality.
The no reflow phenomenon can be diagnosed by serial ECGs.
Background from an older post here.
Recently a medical journalist jumped into the discussion on MOC, criticizing the detractors who have expressed recent outrage about the process. I criticized the piece here, calling out what I thought was a series of straw man arguments. Now the journalist, Larry Husten, has opined again.
He states emphatically in his posts that he is not defending the current MOC process. In fact, in one of his comment threads he says he doesn't even know enough about it to do so. He's not defending the process. Practicing doctors merely want to reform it. It would appear we are in agreement. So why all the fuss? Mr. Husten explains it this way, from the same comment thread:
Remember, I am NOT defending the current MOC system. I don’t know enough about it. I am responding to some of the arguments that have been made against MOC. These ideas strike me as wrong and dangerous and should not go uncorrected simply because everyone else is angry– and perhaps justifiably so– at the current MOC system. In other words, just because the current system may need reform does not justify the use of poor arguments.
The problem is, as I pointed out in my earlier post, Mr. Husten has mischaracterized those arguments. His posts read like attack pieces on the character of practicing doctors. The title of his first post implies that the MOC detractors (who represent the rank-and-file of the profession) are a bunch of crybabies: Three Reasons Why You Don’t Need To Feel Sorry For Doctors. The second title implies that the MOC detractors are wanting immunity from accountability: Why Doctors, Like Airline Pilots, Should Not Be Completely Trusted. Straw man again.
The airline industry analogy, popularized in the early days of the patient safety movement, has since been overstretched. It falls apart on many levels. In using it to build his straw man for the medical profession Mr. Husten does have one valid point in that he seems to be saying that since airline pilots have to be accountable so should doctors:
I would never get on an airplane if I didn’t feel highly confident that the pilot was fully competent. In order to fly a commercial airplane a pilot has to undergo rigorous and continuous training and testing. I’d walk before flying with a pilot whose only credential was his assurance that he’d been diligently “keeping up with his field” and that he was extremely confident in his abilities. I’m glad to know that the FAA and the airlines have extremely demanding programs to ensure the competency of pilots.
Nobody in this discussion disagrees with that.
But a little further down he references my earlier post in this manner:
One of my critics proposed that “it is the individual physicians who should be mainly responsible for their own learning needs, not some group of outsiders.” I wouldn’t get on a plane flown by a pilot who was “mainly responsible” for his or her own learning needs. The same logic is even more true for doctors.
Here the airline pilot comparison falls apart. Airline pilots have a domain of knowledge they have to master. If that's true in medicine it's true in a very different way. Medical knowledge is an ever moving, rapidly expanding target. Over 2000 citations are added to Medline every day. That's why an essential component of the practice of evidence based medicine (EBM) is looking up answers to focused clinical questions at the point of care. This process is widely recognized as a major part of life long learning. And to my earlier point, it has to be done by the individual clinician rather than some outsider because it is centered around a unique patient.
But to say that individual doctors are responsible for their own learning is not to say they are immune from accountability. None of us are asking to make up the questions to our own certifying exams! Accountability must be objective and it must be external. We would all agree with Mr. Husten on that point.
Finally, the conversation up to now has ignored the fact that doctors have accountability structures in place that go way beyond MOC and licensure. In my work in credentialing I deal with other types of certification as well as clinical process and outcome monitoring of physicians which takes place continuously and on many levels.
Palliative care is increasingly being recognized as a part of definitive critical care regardless of prognosis. Review here.
Via Hospital Medicine Virtual Journal Club.
From a recent systematic review:
Background
There are no published clinical consensus guidelines or systematic evaluation supporting the use of corticosteroids for the treatment of cardiac sarcoidosis. The purpose of this study was to systematically review the published data...
Results
A total of 1491 references were retrieved and 10 publications met the inclusion criteria. There were no randomized trials and all publications were of poor to fair quality. In the 10 reports, 257 patients received corticosteroids and 42 patients did not. There were 57 patients with AV conduction disease treated with corticosteroids, with 27/57 (47.4%) improving. In contrast, 16 patients were not treated with corticosteroids and 0/16 improved. Four publications reported on left ventricular function recovery, 2 reported on ventricular arrhythmia burden, and 9 reported on mortality. However, the data quality were too limited to draw conclusions for any of these outcomes.
Conclusions
Our systematic review identified 10 publications reporting outcomes after corticosteroid therapy. The best data relates to AV conduction recovery and corticosteroids appeared to be beneficial. It is not possible to draw clear conclusions about the utility of corticosteroids for the other outcomes. There is a clear need for large multicentre prospective registries and trials in this patient population.
I've blogged this topic a couple of times before. Though the two conditions are superficially similar clinically and electrocardiographically they are completely different pathologically. It makes sense that there would be distinctions evident on close examination. Here is another paper on the electrocariographic differences. From the paper:
T inversion and ST elevation mainly appear in precordial leads and more rarely in limb leads. The duration of ST elevation is short, whereas that of T inversion is long. In some cases, T inversion appears for a while after ST elevation begins, disappears, and then begins to appear again. Differences between these two forms require prospective studies with more patients.
It was also pointed out in the paper that patients with stress cardiomyopathy did not exhibit reciprocal ST depressions whereas sinus tachycardia was common. Note that sinus tachycardia is not generally a manifestation of ACS per se and when present is an ominous sign, signifying acute heart failure or cardiogenic shock.
It can be a powerful tool in large vessel vasculitis, particularly GCA:
Colour Doppler ultrasound displays a pathognomonic circumferential wall thickening in large-vessel vasculitis. Even rather small arteries like the temporal arteries can be easily examined with modern ultrasound equipment. In addition, ultrasound can detect stenoses and acute arterial occlusions. In large-vessel giant cell arteritis, the axillary arteries are most commonly involved. Takayasu arteritis affects particularly the left subclavian and the left common carotid arteries. As ultrasound diagnosis at the temporal arteries becomes more difficult already after a few days of glucocorticoid treatment in some patients, institutions are implementing fast-track clinics for which patients receive an appointment within 24 hours. An experienced rheumatologist is able to establish a definite diagnosis in most cases with standardised history, clinical examination and ultrasound of temporal and axillary arteries. Furthermore, early diagnosis and treatment may prevent blindness.
Via Hospital Medicine Virtual Journal Club.
From a recent review:
Fusarium species is a ubiquitous fungus that causes opportunistic infections. We present 26 cases of invasive fusariosis categorized according to the European Organization for Research and Treatment of Cancer/Mycoses Study Group (EORTC/MSG) criteria of fungal infections. All cases (20 proven and 6 probable) were treated from January 2000 until January 2010. We also review 97 cases reported since 2000. The most important risk factors for invasive fusariosis in our patients were compromised immune system, specifically lung transplantation (n = 6) and hematologic malignancies (n = 5), and burns (n = 7 patients with skin fusariosis), while the most commonly infected site was the skin in 11 of 26 patients. The mortality rates among our patients with disseminated, skin, and pulmonary fusariosis were 50%, 40%, and 37.5%, respectively. Fusarium solani was the most frequent species, isolated from 49% of literature cases. Blood cultures were positive in 82% of both current study and literature patients with disseminated fusariosis, while the remaining 16% had 2 noncontiguous sites of infection but negative blood cultures. Surgical removal of focal lesions was effective in both current study and literature cases.
Skin lesions in immunocompromised patients should raise the suspicion for skin or disseminated fusariosis. The combination of medical monotherapy with voriconazole or amphotericin B and surgery in such cases is highly suggested.
From the green journal:
Methods
Univariate and multivariate analyses were performed using National Health and Nutrition Examination Survey data.
Results
Average body mass index (BMI) increased by 0.37% (95% confidence interval [CI], 0.30-0.44) per year in both women and men. Average waist circumference increased by 0.37% (95% CI, 0.30-0.43) and 0.27% (95% CI, 0.22-0.32) per year in women and men, respectively. The prevalence of obesity and abdominal obesity increased substantially, as did the prevalence of abdominal obesity among overweight adults. Younger women experienced the greatest increases. The proportion of adults who reported no leisure-time physical activity increased from 19.1% (95% CI, 17.3-21.0) to 51.7% (95% CI, 48.9-54.5) in women, and from 11.4% (95% CI, 10.0-12.8) to 43.5% (95% CI, 40.7-46.3) in men. Average daily caloric intake did not change significantly. BMI and waist circumference trends were associated with physical activity level but not caloric intake. The associated changes in adjusted BMIs were 8.3% (95% CI, 6.9-9.6) higher among women and 1.7% (95% CI, 0.68-2.8) higher among men with no leisure-time physical activity compared with those with an ideal level of leisure-time physical activity.
From a recent systematic review:
Data Synthesis: Forty-seven trials were included. Most enrolled adults with moderate to severe HF and a mean age of 70 years. Few trials reported 30-day readmission rates. At 30 days, a high-intensity home-visiting program reduced all-cause readmission and the composite end point (all-cause readmission or death; low SOE). Over 3 to 6 months, home-visiting programs and multidisciplinary heart failure (MDS-HF) clinic interventions reduced all-cause readmission (high SOE). Home-visiting programs reduced HF-specific readmission and the composite end point (moderate SOE). Structured telephone support (STS) interventions reduced HF-specific readmission (high SOE) but not all-cause readmissions (moderate SOE). Home-visiting programs, MDS-HF clinics, and STS interventions produced a mortality benefit. Neither telemonitoring nor primarily educational interventions reduced readmission or mortality rates.
Limitations: Few trials reported 30-day readmission rates. Usual care was heterogeneous and sometimes not adequately described.
Conclusion: Home-visiting programs and MDS-HF clinics reduced all-cause readmission and mortality; STS reduced HF-specific readmission and mortality. These interventions should receive the greatest consideration by systems or providers seeking to implement transitional care interventions for persons with HF.
Full text here.
The document covers first seizure, seizures in patients with a history of epilepsy and status.
Via Intensive care medicine worth knowing.
Heliox is safe and physiologically appealing. It can buy time in certain respiratory emergencies. Its precise role, however, is not well defined by high level studies. Here is an update.
---with disastrous results:
Direct oral factor inhibitors (DOFIs) are an attractive alternative to vitamin K antagonists (VKA) for the treatment of patients with antiphospholipid syndrome (APS). In the absence of prospective, randomised trial data, reports of therapeutic failures in clinical practice alert clinicians to potential limitations of DOFI therapy for this indication. Data for all cases were collected from a centralised system that contains complete medical records of all patients treated and followed at Mayo Medical Center. We present here three consecutive APS patients who had had no thromboembolism recurrence on warfarin but were switched to DOFIs. The diagnosis of APS was established according to currently recommended criteria. The three cases were as follows: A woman with primary APS developed thrombotic endocarditis with symptomatic cerebral emboli after transition to dabigatran. A second woman with primary APS experienced ischemic arterial strokes and right transverse-sigmoid sinus thrombosis after conversion to rivaroxaban. A man with secondary APS suffered porto-mesenteric venous thrombosis after switching to rivaroxaban. None of these patients had failed warfarin prior to the transition to DOFIs. Based on these three cases, we advocate caution in using DOFIs for APS patients outside of a clinical trial setting, until further data becomes available.
This serves as a caution against using these agents outside the clinical situations in which they were studied.
Via Hospital Medicine Virtual Journal Club.
Confusion tends to surround this topic due to different terminologies, overlapping disorders and associated inflammatory diseases both infectious and non-infectious, a notable example of the latter being Still's disease in which it takes the form of macrophage activation syndrome (MAS). Here is an open access review which provides some clarity.
Here is a free full text review from the American Journal of Medicine.
Type 2 MI has received raised awareness but is the subject of a great deal of confusion.
The difference between type 1 MI (ACS due to an unstable coronary plaque) and type 2 MI (myocardial O2 supply/demand imbalance) is often possible on the basis of clinical findings and circumstances.
Another frequent distinction to be made involves the difference between MI (usually type 2) and non ischemic critical illness related troponin elevation. Chest pain, ischemic ECG changes and echocardiographic wall motion abnormalities are absent in the latter condition. (Another cause of troponin elevation that sometimes causes confusion is stress cardiomyopathy. However, it is more likely to mimic STEMI than the conditions described here).
For type 2 MI there is little evidence to drive treatment and no guidelines. Treatment is guided largely by pathophysiologic considerations, focusing on favorably impacting the myocardial oxygen supply and demand balance. From the review:
If a type 2 MI is suspected, the next clinical conundrum develops. Should the patient undergo coronary angiography; should aspirin, a P2Y12 inhibitor, and antithrombotic therapy be administered; should the patient be treated with beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, an angiotensin receptor blocker, a statin, ranolazine, or nitrates? At this time, there is a dearth of scientific information that can help physicians make clinical decisions in this setting. Cardiac catheterBottom Line Available evidence, from underpowered pooled data, neither supports nor refutes an association of systemic antibiotic therapy with improved venous leg ulcer healing. Among topical antimicrobials, cadexomer iodine may be associated with better healing compared with usual care.ization almost certainly is associated with significant risk in such critically ill patients, as is antithrombotic therapy. Often, beta-blockers, nitrates, and low-dose aspirin are given, but without a strong sense on the part of the clinician involved that this therapy is beneficial in this setting. Clinical research involving patients with type 2 MI or myocardial injury is needed desperately to assist in differentiating these 2 entities and determining what, if any, specific therapy is indicated.
In conclusion, the authors feel that careful weighing of the clinical situation is important in guiding further diagnostic testing and possible therapy in patients with type 2 MI or a nonischemic myocardial injury with necrosis. Thus, a patient with one of these syndromes and a poor prognostic outlook might not undergo any further testing following recovery from an acute illness where blood troponin values were elevated, while a patient with a reasonably good prognosis would be offered additional diagnostic evaluation to assess the likelihood of important underlying coronary artery disease and to guide therapy.
A review in the journal Medicine.
From a JAMA Clinical Evidence Synopsis:
Bottom Line Available evidence, from underpowered pooled data, neither supports nor refutes an association of systemic antibiotic therapy with improved venous leg ulcer healing. Among topical antimicrobials, cadexomer iodine may be associated with better healing compared with usual care.
This is a recently emerging entity. We need to learn more about the long term prognosis. In this study a substantial number of patients dropped their EFs again over time. Close long term follow up of these patients is important.
Wellens syndrome has consequences and needs to be recognized early. But the consequences are different now compared to when it was originally described in 1982 due to changes in the cardiology landscape. Back then, lacking sensitive biomarkers and emergency PCI it was an unstable or new angina patient who was a ticking time bomb in need of coronary artery bypass surgery within a matter of days to avert a large anterior MI (the nasty variety complicated by bundle branch block, septal rupture, cardiogenic shock, etc). Now it is framed as a “non-STEMI” nevertheless, generally, in need of a quick trip to the cath lab to avoid a bad outcome. Here's an update at Clinical Correlations.
From an article in Current Opinion in Gastroenterology:
Recent findings: Epidemiological studies have repeatedly described a negative association between H. pylori infection and erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma, but not between H. pylori and gastroesophageal reflux disease symptoms. Especially, infection with CagA-positive strains appears to protect the distal esophagus by causing fundic gland atrophy and impaired gastric acid secretion. Although earlier reports suggested the development of erosive esophagitis after H. pylori eradication, more recent studies discuss that H. pylori eradication usually does not have an important clinical impact on gastroesophageal reflux disease.
Summary: Gastric atrophy is the most widely accepted mechanism by which the distal esophagus is protected from abnormal acid exposure in patients with H. pylori infection. The clinical impact of H. pylori infection on the prevalence of erosive esophagitis and Barrett's esophagus remains a matter of debate. In areas with a high prevalence of H. pylori-induced atrophic gastritis, the protection that this infection may afford against gastroesophageal reflux disease is not comparable to the risk that H. pylori poses for the development of gastric cancer.
Larry Husten is a medical journalist who writes for Cardiobrief, a blog I often link to. Recently he wrote this piece on the maintenance of certification (MOC) debate. The title is a dead giveaway: Three Reasons Why You Don’t Need To Feel Sorry For Doctors. Apparently Husten thinks doctors have little more than whiny arguments to contribute to the discussion. In fact at the end of the article he suggests that the debate has deteriorated to “the ill-tempered ventings of a highly privileged elite.” (Doctors represent a highly privileged elite? On what planet?).
He opens by saying he has no strong opinions on how doctors should be certified but then goes on to express some very strong opinions against the prevailing objections. I'll give him credit for one thing. He correctly points out that there has been very little argument (and, I might add, zero argument of substance) put forth in favor of the recent MOC changes. Instead the specialty boards have just put it out there and said, in effect, “here it is, take it or leave it.”
He goes on to attack three of the objections he says rank-and-file doctors have put forth.
First, that doctors think they are extremely diligent in staying current and therefore don't need MOC. He used as his example a cardiologist interviewed in this Medscape article who in the casual format of the interview wasn't vigilant enough in choosing his words, to make the case that doctors are generally self motivated to stay current. I hope even Mr. Husten would agree with that general premise. But for purposes of his argument he takes the words of the cardiologist literally and carries them to their extreme, thus building a straw man which he can easily ridicule:
Really, Dr. Tierstein? You’ve never met a single physician who had relaxed his standards over time? You’ve never encountered physicians who fail to keep up with important developments? I guess, in your view, all doctors are, like the children of Lake Woebegon, above average.
That is not the argument doctors are making. Husten was stretching the point for purposes of ridicule but I believe I understand what Tierstein was trying to say. The point is that it is the individual physicians who should be mainly responsible for their own learning needs, not some group of outsiders. That's what is known as self assessment and is the original concept, by the way, of MKSAP (which stands for Medical Knowledge Self Assessment Program).
Husten then goes on to build another straw man:
Another argument I’ve heard repeated is that the current continuing medical education (CME) system already provides a perfectly adequate system for MOC.
Again, no one is making the argument that CME is perfectly adequate. Not even Dr. Tierstein in the Medscape interview. In fact, Tierstein's statement about accredited CME is that it is only “pretty good,” not perfect. But Husten rejects even that:
The problem, of course, is that in reality the current CME system is largely funded and controlled by industry...
As I said, CME can play a key role in MOC, but only when the doctors pay for it themselves.
In other words if industry funding is involved there can be no educational value. That's a conveniently simple litmus test but it's empty because there's no evidence of substance to back it up.
The third objection Husten cites is that MOC has not been tested, an argument he dismisses in this manner:
There are many things in life that we all agree are necessary that have not undergone rigorous testing. I’m sure there’s never been a randomized trial demonstrating that 4 years of medical school is better than no medical school, for instance.
No one is asking for a randomized trial. But if you want to add significantly to the already onerous baggage doctors carry you ought to sustain a burden of proof at some level. Medical schools have not been subject to randomized trials but their education offerings have been studied extensively. In fact, entire journals are singularly devoted to studying medical school curricula and holding the educational process accountable. MOC likewise needs to be held accountable.
I usually enjoy Husten's articles and find them informative. Unfortunately, and much to my surprise and disappointment, in this particular post he seems to view doctors involved in the discussion as a bunch of whiners.
---the general rule is not to treat with antifungals. This was recently the subject of a RCT and an observational study.
Methods
We conducted a double-blind, placebo-controlled, multicenter pilot randomized trial of antifungal therapy in critically ill patients with a clinical suspicion of ventilator-associated pneumonia with positive airway secretion specimens for Candida spp. We also included an observational group without Candida spp. in their airway secretions. We measured recruitment rate, inflammatory and innate immune function profiles over time, and clinical outcomes.
Results
We recruited 60 patients into the randomized trial and 29 patients into the observational study. Markers of inflammation and all clinical outcomes were comparable between placebo and antifungal treatment group at baseline and over time. At baseline, plasma TNF-α levels were higher in patients with VAP and Candida compared to the observational group (mean ± SD) (21.8 ± 23.1 versus 12.4 ± 9.3 pg/ml, p = 0.02) and these patients had lower innate immune function as evidenced by reduced whole blood ex vivo LPS-induced TNF-α production capacity (854.8 ± 855.2 versus 1,559.4 ± 1,290.6 pg/ml, p = 0.01).
Conclusions
This study does not provide evidence to support a larger trial examining the efficacy of empiric antifungal treatment in patients with a clinical suspicion of ventilator-associated pneumonia and Candida in the endotracheal secretions. The presence of Candida in the lung may be associated with persistent inflammation and immunosuppression.
Here is a case description and brief discussion in the green journal.
Originally described as a cause of autoimmune pancreatitis, IgG 4 disease has emerged as a multi organ condition.
Elevated IgG 4 can be helpful in making the diagnosis but is present in only 60% of cases. Histopathologic criteria are the most important features in diagnosis.
The condition can affect virtually every organ system and has features of both an autoimmune and allergic (atopic) disorder.
Renal involvement, particularly interstitial nephritis, has been recognized.
This practice parameter document was created by a joint task force in allergy and immunology and is available as free full text (HT to Life in the Fast Lane).
For a little background here is one of my earlier posts on anaphylaxis. And now on to a few of the key points from the document:
The role of serum tryptase measurement
Although a tryptase level is not useful for emergency decision making the authors recommend it be obtained for the information it will provide later, in follow up. Keep in mind that the positive predictive value is only 69%. The reliability of the test varies depending on the source of the anaphylaxis (low sensitivity, for example, when food related) and it is time dependent.
Give IM epi as soon as the clinical diagnosis is made
---acknowledging occasional exceptions, such as when patients present late with resolved or nearly resolved symptoms.
Early fluid resuscitation when circulatory collapse is present
From the document:
Aggressive fluid resuscitation helps to counteract the significant plasma leak associated with anaphylaxis and complement parenteral epinephrine therapy. Children might require successive IV fluid boluses of 20 mL/kg and adults might require successive IV boluses of 1,000 mL to maintain blood pressure in the early stages of anaphylaxis. To overcome venous resistance, fluids administered through IO catheters should be infused under pressure using an infusion pump, pressure bag, or manual pressure.
IM epi doses can be repeated but at some point an epi drip may be necessary for unresponsive patients
5 minute intervals between IM injections are recommended, but open to variation according to clinical judgment. If clinical judgment warrants a drip, 1 mg of epi is diluted in a liter of D5W to give a 1 mcg/ml concentration. The titration range recommended is 1 mcg/min to 10 mcg/min. In more desperate situations:
In patients with actual or impending cardiovascular collapse unresponsive to an epinephrine infusion or when an epinephrine infusion is not immediately available, slow administration of a 50-μg (0.5 mL of 1:10,000) bolus of IV epinephrine might be necessary.
IO access can be used for fluid and epi infusions
Special airway considerations apply
From the document:
Upper airway edema can preclude rescue ventilation, so the merits of an awake fiberoptic intubation should be strongly weighed against the benefits and risks of rapid sequence intubation.
When selecting airway management medications, because patients with anaphylaxis requiring intubation are often hemodynamically unstable, medications should be avoided that depress blood pressure. Paralytics should be used with caution, because mask ventilation can be impossible in the setting of upper airway edema...
Nebulized epinephrine has been shown to alleviate respiratory distress associated with upper airway obstruction in childhood croup.48 The vasoconstrictive (α1) effects likely account for the decrease of upper airway edema. Similarly, and based on anecdotal experience, aerosolized epinephrine also can decrease oropharyngeal edema and make airway management less difficult in anaphylaxis.
What if hypotension is refractory to epi (including a drip) and fluid resuscitation?
Glucagon (1-5 mg over 5 minutes followed by a 5-15 mcg/min infusion) is recommended as the next step. The typical scenario here would be the patient taking beta blockers, since glucagon bypasses the beta receptor. This being said the authors acknowledge, and cite literature, that other pressors have been used successfully.
Consider ECMO if all else fails
See statement 14 from the article.
What about steroids and antihistamines?
They're fine but don't don't put them at the front of the line ahead of epi because they don't work as fast.
From a paper in Resuscitation:
Results
90 patients had CA with an initial rhythm of VF or VT; 65 patients were excluded, leaving 25 for analysis. Six patients received esmolol during cardiac arrest, and nineteen did not. All patients had ventricular dysrhythmias refractory to many defibrillation attempts, including defibrillation after administration of standard ACLS medications. Most received high doses of adrenaline, amiodarone, and sodium bicarbonate. Comparing the patients that received esmolol to those that did not: 67% and 42% had temporary return of spontaneous circulation (ROSC); 67% and 32% had sustained ROSC; 66% and 32% survived to intensive care unit admission; 50% and 16% survived to hospital discharge; and 50% and 11% survived to discharge with a favorable neurologic outcome, respectively.
Conclusion
Beta-blockade should be considered in patients with RVF in the ED prior to cessation of resuscitative efforts.
This is a very small study that would not ordinarily be practice changing but if you're at the point of calling a code for a patient who is still in VF why not? The folks at Academic Life in Emercency Medicine seem to agree.
Based on accumulating experience it would appear that it is. From a recent review:
While regadenoson has become the vasodilator stress agent of choice and has streamlined and simplified stress protocols in many nuclear stress laboratories, the adverse effect of dyspnea is still experienced by many patients, and even more so by those with COPD and asthma. While patients and practitioners should anticipate this symptom, several studies have shown that the subjective experience of dyspnea is not correlated with and is not caused by bronchoconstriction. Available data from observational studies as well as controlled clinical trials, as summarized in Table 1, indicate that the use of regadenoson in patients with mild to moderate asthma and mild to moderate COPD is safe. The current data in patients with severe COPD, while limited, are reassuring and indicate that regadenoson is probably safe, particularly in those with stable lung disease. Clinical data are limited in COPD patients who require 24-hour/day home oxygen administration, have previously been intubated for respiratory failure, or have had recent exacerbations or required uptitration of their medication regimen within a 1-month period; regadenoson should therefore be used with caution in this patient population. Similarly, regadenoson has not been studied in patients with severe bronchial asthma (FEV1 less than 60%); thus, it should be avoided in these patients at this time.
The ultra-cautiously worded statement can be found here:
Results—Patients with CD may present with unilateral headaches, posterior cervical pain, or cerebral or retinal ischemia (transient ischemic or strokes) attributable mainly to artery–artery embolism, CD cranial nerve palsies, oculosympathetic palsy, or pulsatile tinnitus. Diagnosis of CD depends on a thorough history, physical examination, and targeted ancillary investigations. Although the role of trivial trauma is debatable, mechanical forces can lead to intimal injuries of the vertebral arteries and internal carotid arteries and result in CD. Disability levels vary among CD patients with many having good outcomes, but serious neurological sequelae can occur. No evidence-based guidelines are currently available to endorse best management strategies for CDs. Antiplatelet and anticoagulant treatments are both used for prevention of local thrombus and secondary embolism. Case-control and other articles have suggested an epidemiologic association between CD, particularly vertebral artery dissection, and CMT. It is unclear whether this is due to lack of recognition of preexisting CD in these patients or due to trauma caused by CMT. Ultrasonography, computed tomographic angiography, and magnetic resonance imaging with magnetic resonance angiography are useful in the diagnosis of CD. Follow-up neuroimaging is preferentially done with noninvasive modalities, but we suggest that no single test should be seen as the gold standard.
Conclusions—CD is an important cause of ischemic stroke in young and middle-aged patients. CD is most prevalent in the upper cervical spine and can involve the internal carotid artery or vertebral artery. Although current biomechanical evidence is insufficient to establish the claim that CMT causes CD, clinical reports suggest that mechanical forces play a role in a considerable number of CDs and most population controlled studies have found an association between CMT and VAD stroke in young patients.
Carotid or vertebral artery dissection should be considered, especially in youngish patients with stroke symptoms.
This discussion of third nerve palsy at Emergency Physicians Monthly is one of the best I've seen.
From a recent meta-analysis:
The use of short-term high-dose atorvastatin pretreatment is safe and significantly improves the final TIMI flow grade as well as reduces the 30-day MACEs in ACS patients post-PCI. This finding encourages the use of short-term high-dose atorvastatin pretreatment as an alternative for ACS patients undergoing PCI, but more high-quality randomized clinical trials are still needed to confirm the long-term efficacy and safety.
The document incorporates the new findings from ProCESS and ARISE and emphasizes the emerging role of bedside echocardiography in the hemodynamic assessment of patients in shock. Available here as free full text.
More from Intensive Care Medicine-Working Knowledge.
