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.
Saturday, January 31, 2015
Obesity as a driver of cardiovascular disease: inflammatory mechanisms
From a recent review:
Friday, January 30, 2015
Rendu-Osler-Weber disease
This brief review discusses the consequences of pulmonary AV shunting. Free full text.
Thursday, January 29, 2015
Hypertension management in stroke patient post discharge
From a new paper in Stroke:
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.
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.
Parkinson's disease in the perioperative period: what the hospitalist needs to know
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.
Wednesday, January 28, 2015
NEJM perspective piece on maintenance of certification
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:
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.
Cannabis and cardiovascular risk
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.
Tuesday, January 27, 2015
Dr. Lawrence Weed and the problem oriented medical record
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.
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.
Medscape interview on maintenance of certification (MOC)
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.
Precocious acute coronary syndrome
From a recent study of very young patients presenting with ACS:
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.
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.
Monday, January 26, 2015
Case presentation: a “non STEMI” that wasn't and the no reflow phenomenon
The conversation on maintenance of certification (MOC) continues
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:
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:
Nobody in this discussion disagrees with that.
But a little further down he references my earlier post in this manner:
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.
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.
Sunday, January 25, 2015
Palliative care in the ICU
Palliative care is increasingly being recognized as a part of definitive critical care regardless of prognosis. Review here.
Via Hospital Medicine Virtual Journal Club.
Via Hospital Medicine Virtual Journal Club.
Are corticosteroids beneficial for cardiac sarcoidosis?
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.
Saturday, January 24, 2015
Friday, January 23, 2015
The ECG in stress cardiomyopathy versus acute coronary syndrome
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:
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.
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.
Thursday, January 22, 2015
The use of ultrasound in the diagnosis of vasculitis
It can be a powerful tool in large vessel vasculitis, particularly GCA:
Via Hospital Medicine Virtual Journal Club.
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.
Wednesday, January 21, 2015
Fusarium infections
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.
Tuesday, January 20, 2015
Trends in physical activity and obesity
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.
Which interventions are most effective in reducing heart failure admissions and mortality?
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.
Monday, January 19, 2015
Seizure guidelines for emergency medicine
Full text here.
The document covers first seizure, seizures in patients with a history of epilepsy and status.
Via Intensive care medicine worth knowing.
The document covers first seizure, seizures in patients with a history of epilepsy and status.
Via Intensive care medicine worth knowing.
Heliox in critical care
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.
Sunday, January 18, 2015
Failures of target specific oral anticoagulants (TSOACs) in patients with antiphospholipid syndrome
---with disastrous results:
This serves as a caution against using these agents outside the clinical situations in which they were studied.
Via Hospital Medicine Virtual Journal Club.
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.
Hemophagocytic lymphohistiocytosis
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.
Saturday, January 17, 2015
Type 2 MI
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:
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.
Friday, January 16, 2015
Antibiotics for venous leg ulcers?
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.
Heart failure with recovered ejection fraction (HF-REF)
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.
Thursday, January 15, 2015
Wellens syndrome in 2015
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.
The paradox of H pylori and GERD
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.
Wednesday, January 14, 2015
A non-physician weighs in on maintenance of certification
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:
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:
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:
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:
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.
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.
When Candida grows in respiratory secretions
---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.
IgG 4 related systemic disease
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.
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.
Tuesday, January 13, 2015
Diagnosis and management of anaphylaxis
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:
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:
IO access can be used for fluid and epi infusions
Special airway considerations apply
From the document:
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.
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.
Esmolol for cardiac arrest?
From a paper in Resuscitation:
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.
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.
Regadenoson (Lexiscan) stress testing in patients with COPD and asthma: is it safe?
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.
Monday, January 12, 2015
Neck manipulation and stroke: a scientific statement from AHA
The ultra-cautiously worded statement can be found here:
Carotid or vertebral artery dissection should be considered, especially in youngish patients with stroke symptoms.
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.
Third nerve palsy
This discussion of third nerve palsy at Emergency Physicians Monthly is one of the best I've seen.
Short term high dose statin use in acute coronary syndrome
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.
Sunday, January 11, 2015
European Society of Intensive Care Medicine consensus on shock
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.
More from Intensive Care Medicine-Working Knowledge.
From the Clinician Update series: Long QT syndrome
Free full text review in Circulation. Via Hospital Medicine Virtual Journal Club.
Saturday, January 10, 2015
On the diagnosis of heart failure
The diagnosis of heart failure is of consequence to hospitalists. It can easily be confused with other conditions that cause dyspnea, weakness, edema and lung opacities. The regulatory environment drives a rush toward a specific diagnostic label. When heart failure is diagnosed in error harm may result as inappropriate core measures and care pathways are triggered. There is a certain amount of leeway for throwing labels around. For example, to stretch the point, according to the ABCD classification anyone with hypertension or diabetes but no structural heart disease or cardiac symptoms has heart failure stage A. In the day to day clinical world certain tests such as echocardiography and BNP are inappropriately used as surrogates for clinical assessment. So how should the hospitalist approach this?
The most practical definition of heart failure is that of a clinical syndrome, so its diagnosis is primarily a clinical one. The Framingham criteria may be the best starting point. BNP testing is ancillary. It has utility in helping differentiate heart failure from other causes of dyspnea when the findings are unclear. Echocardiography, rather than a tool to diagnose heart failure, is indicated to assess for certain forms of structural heart disease and to categorize the heart failure syndrome physiologically, thus guiding treatment.
The most practical definition of heart failure is that of a clinical syndrome, so its diagnosis is primarily a clinical one. The Framingham criteria may be the best starting point. BNP testing is ancillary. It has utility in helping differentiate heart failure from other causes of dyspnea when the findings are unclear. Echocardiography, rather than a tool to diagnose heart failure, is indicated to assess for certain forms of structural heart disease and to categorize the heart failure syndrome physiologically, thus guiding treatment.
Immune deficiency disorders in adults: what the hospitalist needs to know
Here is a great review in ACP hospitaliast.
Measles in critically ill adults---nothing measly about it
From a recent Medicine review:
France has recently witnessed a nationwide outbreak of measles...We performed a retrospective analysis of a cohort of 36 adults admitted to a total of 64 ICUs throughout France for complications of measles...
Among the 26 patients whose measles vaccination status was documented, none had received 2 injections. One patient had developed measles during childhood. Underlying comorbid conditions included chronic respiratory disease in 9 patients, immunosuppression in 7 patients, and obesity in 3 patients, while measles affected 5 pregnant women.
Respiratory complications induced by measles infection led to ICU admission in 32 cases, and measles-related neurologic complications led to ICU admission in 2 cases. Two patients were admitted due to concurrent respiratory and neurologic complications...
Measles is a disease with protean and potentially deceptive clinical manifestations, especially in the immunocompromised patient. Measles-associated pneumonitis and its complications, and less commonly postinfectious encephalomyelitis, are the main source of morbidity and mortality. In contrast with the usually benign course of the disease in immunocompetent patients, measles occurring in immunocompromised patients gives rise to lethal complications including ARDS, with or without bacterial superinfection. Other patients potentially at high risk for severe measles are young adults and pregnant women. Measles pneumonitis may predispose to air leak disease in patients using mechanical ventilation. To date, vaccination remains the most potent tool to control measles infection.
Friday, January 09, 2015
Wake up and breathe protocols: time to rethink?
In view of the recent trends toward lighter sedation the evidence gets a critical look in this post.
Principles of IV fluid therapy
This review conceptualizes four phases of fluid therapy in critically ill patients:
The first two components in this model were lumped together in the three phase concept I recently discussed here. Both models emphasize that in the final phase fluid is removed in order to restore neutral balance, either passively or with the use of diuretics.
Via Intensive Care Medicine-Working Knowledge.
The framework recently proposed by Vincent and De Backer16 recognizes four distinct phases or stages of resuscitation: Rescue, Optimization, Stabilization, and De-escalation (ROS-D)...
The Rescue phase anticipates an immediate escalation of fluid therapy, for resuscitation of the patient with life-threatening shock (characterized by low arterial pressure, signs of impaired perfusion, or both), and characterized by the use of fluid bolus therapy (see Box 2). In Optimization, the patient is no longer in immediate life-threatening danger but is in a stage of compensated shock (but at high risk of decompensation) and any additional fluid therapy is given more cautiously, and titrated with the aim of optimizing cardiac function to improve tissue perfusion with ultimate goal of mitigating organ dysfunction. The workgroup felt strongly that a clear distinction had to be made between a ‘fluid bolus’, that is, large volume given rapidly to rescue, without close monitoring, and a ‘fluid challenge’ …
Stabilization reflects the point at which a patient is in a steady state so that fluid therapy is now only used for ongoing maintenance …
Finally, while in the first three stages (‘SOS’), fluids are usually administered, in the last stage (D), fluids will also be removed from the patient and usually, the goal will be to promote a negative fluid balance (Fig. 2)...
The first two components in this model were lumped together in the three phase concept I recently discussed here. Both models emphasize that in the final phase fluid is removed in order to restore neutral balance, either passively or with the use of diuretics.
Via Intensive Care Medicine-Working Knowledge.
Non invasive positive pressure ventilation has emerged in prime time
As if we didn't already know that, here's a paper documenting recent trends in use. It concludes:
Conclusions: NIV occupies an important role in the management of acute respiratory failure in acute care hospitals in selected US hospitals and is being used for a large majority of patients with acute-on-chronic respiratory failure and acute cardiogenic pulmonary edema. NIV use appears to have increased substantially in selected US hospitals over the past decade.
Thursday, January 08, 2015
How effectively do clinicians access answers to clinical questions at the point of care?
From a recent systematic review (my italics):
I would like to know what evidence supports that last statement.
Objective To systematically review studies that examined the questions clinicians raise in the context of patient care decision making...
Results In 11 studies, 7012 questions were elicited through short interviews with clinicians after each patient visit. The mean frequency of questions raised was 0.57 (95% CI, 0.38-0.77) per patient seen, and clinicians pursued 51% (36%-66%) of questions and found answers to 78% (67%-88%) of those they pursued. Overall, 34% of questions concerned drug treatment, and 24% concerned potential causes of a symptom, physical finding, or diagnostic test finding. Clinicians’ lack of time and doubt that a useful answer exists were the main barriers to information seeking.
Conclusions and Relevance Clinicians frequently raise questions about patient care in their practice. Although they are effective at finding answers to questions they pursue, roughly half of the questions are never pursued. This picture has been fairly stable over time despite the broad availability of online evidence resources that can answer these questions. Technology-based solutions should enable clinicians to track their questions and provide just-in-time access to high-quality evidence in the context of patient care decision making. Opportunities for improvement include the recent adoption of electronic health record systems and maintenance of certification requirements.
I would like to know what evidence supports that last statement.
Wednesday, January 07, 2015
Tuesday, January 06, 2015
Treatment options for carbapenem-resistant Enterobacteriaceae
Here's an update of recent literature:
Recent findings Retrospective and prospective (nonrandomized noncontrolled) studies provide data regarding the management of infections due to carbapenem-resistant Enterobacteriaceae. The combination of a carbapenem with colistin or high-dose tigecycline or aminoglycoside or even triple carbapenem-containing combinations if the minimum inhibitory concentration (MIC) range of carbapenem (meropenem and imipenem) resistance is 8 mg/l or less seems to have an advantage over monotherapy with either colistin or tigecycline or fosfomycin. For Enterobacteriaceae with MIC for carbapenems over 8 mg/l, combination regimens involve colistin, tigecycline usually administered in a double dose than that suggested by its manufacturer, fosfomycin and aminoglycosides in various combinations.
Summary Suggestions based on the limited literature cannot be made safely. Combination regimens involving carbapenems for Enterobacteriaceae with MICs 8 mg/l or less for carbapenems (in dual combination with colistin or high-dose tigecycline or aminoglycoside or even triple combinations) seem to confer some therapeutic advantage over monotherapy. For Enterobacteriaceae with higher than the above-mentioned MICs, a combination of two or even three antibiotics among colistin, high-dose tigecycline, aminoglycoside and fosfomycin seems to confer decreased mortality.
Pulmonary hypertension in chronic lung disease
From a State-of-the-Art paper in JACC:
The prevalence of pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD) depends on the severity of the disease and the definition of PH (see discussion in the following text). Several studies in patients with the previous GOLD (Global Initiative for Chronic Obstructive Lung Disease) stage IV showed that up to 90% of these patients have a mean pulmonary artery pressure (mPAP) of greater than 20 mm Hg, with most ranging between 20 and 35 mm Hg and ∼3% to 5% patients with mPAP greater than 35 to 40 mm Hg...
In idiopathic pulmonary fibrosis (IPF), which has a survival range of only 2.5 to 3.5 years, mPAP values of greater than 25 mm Hg were reported in 8.1% and 14.9% of patients, respectively, upon initial workup (9,). Higher percentages are found in advanced (30% to 50%) and end-stage (greater than 60%) IPF cases (11,12,13). Among these, a small percentage may present with mPAP values greater than 40 mm Hg (∼9% 14)...
Combined pulmonary fibrosis and emphysema (CPFE) patients are particularly prone to PH development, with estimates approaching 30% to 50%.
Monday, January 05, 2015
Sunday, January 04, 2015
Risk factors for persistent or permanent atrial fibrillation versus paroxysmal atrial fibrillation
Some data from the Women's Health Study:
Related post here.
Background Once atrial fibrillation (AF) progresses to sustained forms, adverse outcomes increase and treatment success rates decrease. Therefore, identification of risk factors predisposing to persistence of AF may have a significant impact on AF morbidity.
Methods and Results We prospectively examined the differential associations between traditional, lifestyle, and biomarker AF risk factors and development of paroxysmal versus nonparoxysmal AF (persistent/permanent) among 34 720 women enrolled in the Women's Health Study who were free of cardiovascular disease and AF at baseline...In multivariable time‐varying competing risk models, increasing age (hazard ratio [HR] 1.11, 95% CI 1.10 to 1.13, versus HR 1.08, 1.07 to 1.09, per year), body mass index (HR 1.07, 1.05 to 1.09, versus HR 1.03, 1.02 to 1.05, per kg/m2), and weight (HR 1.30, 1.22 to 1.39, versus HR 1.14, 1.08 to 1.20, per 10 kg) were more strongly associated with the development of nonparoxysmal AF compared with paroxysmal AF. Hemoglobin A1c levels at baseline were directly related to the development of nonparoxysmal AF but inversely associated with paroxysmal AF in multivariable competing risk models (P for nonequal association=0.01).
Conclusions In women without AF or CVD at baseline, increasing age, adiposity, and higher hemoglobin A1c levels were preferentially associated with the early development of nonparoxysmal AF. These data raise the hypothesis that efforts aimed at weight reduction or glycemic control may affect the proportion of the population with sustained AF.
Related post here.
Antibiotic stewardship: tips and pointers
This article discusses the overuse of antibiotics. True cellulitis versus cellulitis mimics, over diagnosis and treatment of UTI, true sepsis versus non-infectious SIRS and distinguishing true bacteremia from blood culture contaminants are among the issues discussed.
Saturday, January 03, 2015
Friday, January 02, 2015
Clostridium difficile guidelines
Guidelines are available from the Infectious Disease Society of America and the American College of Gastroenterology.
Here are some points of interest from the guidelines. These represent an oversimplification and readers are referred to the original documents, which are available at the above links as free full text. The IDSA version is a bit dated but an update is anticipated next year. Therefore the comments below focus mainly on the ACG guidelines.
The two guidelines differ slightly in their categorizations of severity of disease.
Severe disease is defined as leukocytosis (15,000) OR cr of 1.5 X baseline in the IDSA document; it is defined as albumin below 3 AND either leukocytosis (15,000) or abdominal tenderness according to ACG. Both guidelines denote the additional category of severe-complicated for patients with severe disease plus either findings of hypoperfusion (in terms of blood pressure or lactic acid level) or evidence of gut functional disturbance that calls for added alternative means of drug delivery (ileus, megacolon).
The treatment recommendations are similar in both guidelines.
Mild disease: metronidazole 500 mg PO TID.
Severe disease: vancomycin 125 mg PO QID.
Severe-complicated: vancomycin 500 mg PO or NG QID plus metronidazole 500 mg IV Q8H with or without vanc enemas.
The ACG guideline mentions the FDA approval of fidaxomicin but does not include it in the treatment recommendations.
Fecal transplant is recommended for consideration in the event of a third recurrence.
The guideline does cite the NEJM study from last year and noted an NIH sponsored trial which is underway, looking at patients with a second recurrence.
Patients with inflammatory bowel disease (IBD) hospitalized with a flare should be tested for C diff.
Immunosuppressive treatment can continue in IBD patients infected with C diff provided adequate treatment for the C diff is in place.
IBD patients with a severe colitis flare should be considered for expectant C diff treatment pending test results, as should any patient in which there is a strong clinical suspicion.
Potentially inciting antibiotics should be stopped if possible.
What if concomitant antibiotics can't be stopped? According to this study they don't preclude successful treatment but they are associated with modestly lower cure rates, longer time to resolution and an increased relapse rate. The study results suggested that fidaxomicin was superior in that situation.
Here are some points of interest from the guidelines. These represent an oversimplification and readers are referred to the original documents, which are available at the above links as free full text. The IDSA version is a bit dated but an update is anticipated next year. Therefore the comments below focus mainly on the ACG guidelines.
The two guidelines differ slightly in their categorizations of severity of disease.
Severe disease is defined as leukocytosis (15,000) OR cr of 1.5 X baseline in the IDSA document; it is defined as albumin below 3 AND either leukocytosis (15,000) or abdominal tenderness according to ACG. Both guidelines denote the additional category of severe-complicated for patients with severe disease plus either findings of hypoperfusion (in terms of blood pressure or lactic acid level) or evidence of gut functional disturbance that calls for added alternative means of drug delivery (ileus, megacolon).
The treatment recommendations are similar in both guidelines.
Mild disease: metronidazole 500 mg PO TID.
Severe disease: vancomycin 125 mg PO QID.
Severe-complicated: vancomycin 500 mg PO or NG QID plus metronidazole 500 mg IV Q8H with or without vanc enemas.
The ACG guideline mentions the FDA approval of fidaxomicin but does not include it in the treatment recommendations.
Fecal transplant is recommended for consideration in the event of a third recurrence.
The guideline does cite the NEJM study from last year and noted an NIH sponsored trial which is underway, looking at patients with a second recurrence.
Patients with inflammatory bowel disease (IBD) hospitalized with a flare should be tested for C diff.
Immunosuppressive treatment can continue in IBD patients infected with C diff provided adequate treatment for the C diff is in place.
IBD patients with a severe colitis flare should be considered for expectant C diff treatment pending test results, as should any patient in which there is a strong clinical suspicion.
Potentially inciting antibiotics should be stopped if possible.
What if concomitant antibiotics can't be stopped? According to this study they don't preclude successful treatment but they are associated with modestly lower cure rates, longer time to resolution and an increased relapse rate. The study results suggested that fidaxomicin was superior in that situation.
Dental procedures and antiplatelet agents
From the green journal:
In patients taking antiplatelet medications who are undergoing dental surgery, physicians and dentists must weigh the bleeding risks in continuing antiplatelet medications versus the thrombotic risks in interrupting antiplatelet medications. Bleeding complications requiring more than local measures for hemostasis are rare after dental surgery in patients taking antiplatelet medications. Conversely, the risk for thrombotic complications after interruption of antiplatelet therapy for dental procedures apparently is significant, although small. When a clinician is faced with a decision to continue or interrupt antiplatelet therapy for a dental surgical patient, the decision comes down to “bleed or die.” That is, there is a remote chance that continuing antiplatelet therapy will result in a (nonfatal) bleeding problem requiring more than local measures for hemostasis versus a small but significant chance that interrupting antiplatelet therapy will result in a (possibly fatal) thromboembolic complication. The decision is simple: It is time to stop interrupting antiplatelet therapy for dental surgery.
Subscribe to:
Posts (Atom)