Saturday, March 16, 2019
P wave indices and risk of ischemic stroke
Conclusions—P-wave terminal force in lead V1, P-wave duration, and maximum P-wave area are useful electrocardiographic markers that can be used to stratify the risk of incident ischemic stroke.
Friday, March 15, 2019
Spontaneous pneumothorax (apparent primary spontaneous pneumothorax) may be the first clue to certain cystic lung diseases
Abstract:
Purpose of review: Diffuse cystic lung diseases (DCLDs) are a heterogeneous group of disorders with varying pathophysiologic mechanisms that are characterized by the presence of air-filled lung cysts. These cysts are prone to rupture, leading to the development of recurrent spontaneous pneumothoraces. In this article, we review the epidemiology, clinical features, and management DCLD-associated spontaneous pneumothorax, with a focus on lymphangioleiomyomatosis, Birt–Hogg–Dubé syndrome, and pulmonary Langerhans cell histiocytosis.
Recent findings: DCLDs are responsible for approximately 10% of apparent primary spontaneous pneumothoraces. Computed tomography screening for DCLDs (Birt–Hogg–Dubé syndrome, lymphangioleiomyomatosis, and pulmonary Langerhans cell histiocytosis) following the first spontaneous pneumothorax has recently been shown to be cost-effective and can help facilitate early diagnosis of the underlying disorders. Patients with DCLD-associated spontaneous pneumothorax have a very high rate of recurrence, and thus pleurodesis should be considered following the first episode of spontaneous pneumothorax in these patients, rather than waiting for a recurrent episode. Prior pleurodesis is not a contraindication to future lung transplant.
Summary: Although DCLDs are uncommon, spontaneous pneumothorax is often the sentinel event that provides an opportunity for diagnosis. By understanding the burden and implications of pneumothoraces in DCLDs, clinicians can facilitate early diagnosis and appropriate management of the underlying disorders.
Emerging long term risks of proton pump inhibitors
First introduced in 1989, proton pump inhibitors (PPIs) are among the most widely utilized medications worldwide, both in the ambulatory and inpatient clinical settings. The PPIs are currently approved by the US Food and Drug Administration for the management of a variety of gastrointestinal disorders including symptomatic peptic ulcer disease, gastroesophageal reflux disease, and nonulcer dyspepsia as well as for prevention of gastrointestinal bleeding in patients receiving antiplatelet therapy. PPIs inhibit gastric acid secretion, and the most commonly associated adverse effects include abdominal pain, diarrhea, and headache. Although PPIs have had an encouraging safety profile, recent studies regarding the long-term use of PPI medications have noted potential adverse effects, including risk of fractures, pneumonia, Clostridium difficile diarrhea, hypomagnesemia, vitamin B12 deficiency, chronic kidney disease, and dementia. These emerging data have led to subsequent investigations to assess these potential risks in patients receiving long-term PPI therapy. However, most of the published evidence is inadequate to establish a definite association between PPI use and the risk for development of serious adverse effects. Hence, when clinically indicated, PPIs can be prescribed at the lowest effective dose for symptom control.
Thursday, March 14, 2019
Early arterial ischemic events after VTE in cancer patients
•Arterial events are a major cause of death in cancer patients with venous thrombosis.•Arterial events occur early after venous thrombosis in cancer patients.•The risk of arterial events should be considered in this clinical setting.
Abstract
Background
Venous thromboembolism is common in patients with malignancies, affecting up to 10% of this patient population. The association between arterial ischemic events and venous thromboembolism also has been established. However, the influence of arterial ischemic events on outcomes in cancer patients with venous thromboembolism has not been fully determined.
Methods
The current study analyzed clinical characteristics, time course, risk factors, incidence and severity of venous thromboembolism recurrences, arterial ischemic events and major bleeding in 5717 patients with active cancer and venous thromboembolism recruited into RIETE (multi-center prospective registry of patients with objectively confirmed venous thromboembolism).
Results
During the anticoagulation course (median 7.3 months), 499 (8.7%) patients developed venous thromboembolism recurrences, 63 (1.1%) developed arterial events, and 346 (6.1%) suffered from major bleeding. Overall, major bleeding and arterial events appeared earlier (median 35 and 36 days, respectively) than venous thromboembolism recurrences (median 97 days). Thirty-day mortality rates after each event were: 20% after recurrent pulmonary embolism, 13% after recurrent deep vein thrombosis, 41% after major bleeding, 40% after myocardial infarction, 64% after ischemic stroke, and 83% after lower limb amputation. Bleeding was the leading cause of death (67 fatal bleeds), whereas cumulative mortality due to arterial ischemic events (n = 27) was similar to that related to pulmonary embolism recurrences (n = 26).
Conclusions
In this study, arterial ischemic events and major bleeding appeared early after venous thromboembolism in patients with active cancer and were among frequent causes of their deaths. The risk and severity of arterial events need to be considered in this clinical setting.
ARDS: are we making a dent?
An analysis of
ARDSnet trials shows declining mortality since 1996:
Objectives: There has been multiple advances in the management of acute respiratory distress syndrome, but the temporal trends in acute respiratory distress syndrome–related mortality are not well known. This study aimed to investigate the trends in mortality in acute respiratory distress syndrome patients over time and to explore the roles of daily fluid balance and ventilation variables in those patients.
Design: Secondary analysis of randomized controlled trials conducted by the Acute Respiratory Distress Syndrome Network from 1996 to 2013.
Setting: Multicenter study involving Acute Respiratory Distress Syndrome Network trials.
Patients: Patients with acute respiratory distress syndrome.
Interventions: None.
Measures and Main Results: Individual patient data from 5,159 acute respiratory distress syndrome patients (excluding the Late Steroid Rescue Study trial) were enrolled in this study. The crude mortality rate decreased from 35.4% (95% CI, 29.9–40.8%) in 1996 to 28.3% (95% CI, 22.0–34.7%) in 2013. By adjusting for the baseline Acute Physiology and Chronic Health Evaluation III, age, ICU type, and admission resource, patients enrolled from 2005 to 2010 (odds ratio, 0.61; 95% CI, 0.50–0.74) and those enrolled after 2010 (odds ratio, 0.73; 95% CI, 0.58–0.92) were associated with lower risk of death as compared to those enrolled before 2000. The effect of year on mortality decline disappeared after adjustment for daily fluid balance, positive end-expiratory pressure, tidal volume, and plateau pressure. There were significant trends of declines in daily fluid balance, tidal volume, and plateau pressure and an increase in positive end-expiratory pressure over the 17 years.
Conclusions: Our study shows an improvement in the acute respiratory distress syndrome-related mortality rate in the critically ill patients enrolled in the Acute Respiratory Distress Syndrome Network trials. The effect was probably mediated via decreased tidal volume, plateau pressure, and daily fluid balance and increased positive end-expiratory pressure.
Wednesday, March 13, 2019
Amp-C beta lactamase producing organisms
From a recent
review:
BACKGROUND:
Enterobacterales are among the most common causes of bacterial infections in the community and among hospitalized patients, and multidrug-resistant (MDR) strains have emerged as a major threat to human health. Resistance to third-generation cephalosporins is typical of MDRs, being mainly due to the production of extended spectrum β-lactamases or AmpC-type β-lactamases.
OBJECTIVE:
The objective of this paper is to review the epidemiological impact, diagnostic issues and treatment options with AmpC producers.
FINDINGS:
AmpC enzymes encoded by resident chromosomal genes (cAmpCs) are produced by some species (e.g., Enterobacter spp., Citrobacter freundii, Serratia marcescens), while plasmid-encoded AmpCs (pAmpCs) can be encountered also in species that normally do not produce cAmpCs (e.g., Salmonella enterica, Proteus mirabilis, Klebsiella pneumoniae and Klebsiella oxytoca) or produce them at negligible levels (e.g., Escherichia coli). Production of AmpCs can be either inducible or constitutive, resulting in different resistance phenotypes. Strains producing cAmpCs in an inducible manner (e.g., Enterobacter spp.) usually appear susceptible to third-generation cephalosporins, which are poor inducers, but can easily yield mutants constitutively producing the enzyme which are resistant to these drugs (which are good substrates), resulting in treatment failures. pAmpCs are usually constitutively expressed. Production of pAmpCs is common in community-acquired infections, while cAmpC producers are mainly involved in healthcare-associated infections.
CONCLUSIONS:
To date, there is no conclusive evidence about the most appropriate treatment for AmpC-producing Enterobacterales. Carbapenems are often the preferred option, especially for severe infections in which adequate source control is not achieved, but cefepime is also supported by substantial clinical evidences as an effective carbapenem-sparing option.
Autoimmune thyroid disease
Free full text review. From the conclusion:
The management of autoimmune thyroid disease continues to be revised by new research which includes the identification of new entities, such as IgG4-related thyroid disease and new drug-induced forms of thyroid disease; the development of novel small molecules capable of influencing mechanisms of autoimmunity; and more detailed knowledge of the risks versus benefits of thyroxine therapy in subclinical hypothyroidism.
Tuesday, March 12, 2019
The relationship between atrial fibrillation and dementia
Reviewed in the green journal. It is unclear the extent to which it may be
driven by factors other than stroke.
Trends in the use of ACLS drugs
Objectives: Clinical providers have access to a number of pharmacologic agents during in-hospital cardiac arrest. Few studies have explored medication administration patterns during in-hospital cardiac arrest. Herein, we examine trends in use of pharmacologic interventions during in-hospital cardiac arrest both over time and with respect to the American Heart Association Advanced Cardiac Life Support guideline updates.
Design: Observational cohort study.
Setting: Hospitals contributing data to the American Heart Association Get With The Guidelines–Resuscitation database between 2001 and 2016.
Patients: Adult in-hospital cardiac arrest patients.
Interventions: The percentage of patients receiving epinephrine, vasopressin, amiodarone, lidocaine, atropine, bicarbonate, calcium, magnesium, and dextrose each year were calculated in patients with shockable and nonshockable initial rhythms. Hierarchical multivariable logistic regression was used to determine the annual adjusted odds of medication administration. An interrupted time series analysis was performed to assess change in atropine use after the 2010 American Heart Association guideline update.
Measurements and Main Results: A total of 268,031 index in-hospital cardiac arrests were included. As compared to 2001, the adjusted odds ratio of receiving each medication in 2016 were epinephrine (adjusted odds ratio, 1.5; 95% CI, 1.3–1.8), vasopressin (adjusted odds ratio, 1.5; 95% CI, 1.1–2.1), amiodarone (adjusted odds ratio, 3.4; 95% CI, 2.9–4.0), lidocaine (adjusted odds ratio, 0.2; 95% CI, 0.2–0.2), atropine (adjusted odds ratio, 0.07; 95% CI, 0.06–0.08), bicarbonate (adjusted odds ratio, 2.0; 95% CI, 1.8–2.3), calcium (adjusted odds ratio, 2.0; 95% CI, 1.7–2.3), magnesium (adjusted odds ratio, 2.2; 95% CI, 1.9–2.7; p less than 0.0001), and dextrose (adjusted odds ratio, 2.8; 95% CI, 2.3–3.4). Following the 2010 American Heart Association guideline update, there was a downward step change in the intercept and slope change in atropine use (p less than 0.0001).
Conclusions: Prescribing patterns during in-hospital cardiac arrest have changed significantly over time. Changes to American Heart Association Advanced Cardiac Life Support guidelines have had a rapid and substantial effect on the use of a number of commonly used in-hospital cardiac arrest medications.
Note the increased
usage of bicarb and calcium. These are niche agents which are
critically important in limited situations but have no place in the
routine management of arrest. It is concerning that their use has
increased despite being removed from ACLS protocols decades ago with
a lack of high level evidence of benefit, possible evidence of harm,
and the current bicarb shortage.
Effect of angiotensin II in patients with vasodilatory (mainly septic) shock requiring renal replacement therapy
Objective: Acute kidney injury requiring renal replacement therapy in severe vasodilatory shock is associated with an unfavorable prognosis. Angiotensin II treatment may help these patients by potentially restoring renal function without decreasing intrarenal oxygenation. We analyzed the impact of angiotensin II on the outcomes of acute kidney injury requiring renal replacement therapy.
Design: Post hoc analysis of the Angiotensin II for the Treatment of High-Output Shock 3 trial.
Setting: ICUs.
Patients: Patients with acute kidney injury treated with renal replacement therapy at initiation of angiotensin II or placebo (n = 45 and n = 60, respectively).
Interventions: IV angiotensin II or placebo.
Measurements and Main Results: Primary end point: survival through day 28; secondary outcomes included renal recovery through day 7 and increase in mean arterial pressure from baseline of greater than or equal to 10 mm Hg or increase to greater than or equal to 75 mm Hg at hour 3. Survival rates through day 28 were 53% (95% CI, 38%–67%) and 30% (95% CI, 19%–41%) in patients treated with angiotensin II and placebo (p = 0.012), respectively. By day 7, 38% (95% CI, 25%–54%) of angiotensin II patients discontinued RRT versus 15% (95% CI, 8%–27%) placebo (p = 0.007). Mean arterial pressure response was achieved in 53% (95% CI, 38%–68%) and 22% (95% CI, 12%–34%) of patients treated with angiotensin II and placebo (p = 0.001), respectively.
Conclusions: In patients with acute kidney injury requiring renal replacement therapy at study drug initiation, 28-day survival and mean arterial pressure response were higher, and rate of renal replacement therapy liberation was greater in the angiotensin II group versus the placebo group. These findings suggest that patients with vasodilatory shock and acute kidney injury requiring renal replacement therapy may preferentially benefit from angiotensin II.
Monday, March 11, 2019
Procalcitonin monitoring can help shorten the duration of antibiotic therapy in pneumonia
Abstract:
Purpose of review: Increasing antimicrobial resistance is a worldwide phenomenon that is threatening public health. Lower respiratory infections are one of the leading causes of morbidity that contribute to antibiotic consumption and thus the emergence of multidrug-resistant microbial strains. The goal of shortening antibiotic regimens’ duration in common bacterial infections has been prioritized by antimicrobial stewardship programs as an action against this problem.
Recent findings: Data coming from randomized controlled trials, meta-analyses, and systematic reviews support the shortening of antimicrobial regimens in community-acquired, hospital-acquired, and ventilator-associated pneumonia. Short schedules have been proven at least as effective as long ones in terms of antimicrobial-free days and clinical cure. Procalcitonin-based algorithms have been validated as well tolerated and cost-effective tools for the duration of pneumonia therapy reduction.
Summary: Shortening the duration of antibiotic regimens in pneumonia seems a reasonable strategy for reducing selective pressure driving antimicrobial resistance and costs provided that clinical cure is guaranteed. Procalcitonin-based protocols have been proven essentially helpful in this direction.
Can procalcitonin help predict the microbiology of community acquired pneumonia?
Abstract
Background.
Recent trials suggest procalcitonin-based guidelines can reduce antibiotic use for respiratory infections. However, the accuracy of procalcitonin to discriminate between viral and bacterial pneumonia requires further dissection.
Methods.
We evaluated the association between serum procalcitonin concentration at hospital admission with pathogens detected in a multicenter prospective surveillance study of adults hospitalized with community-acquired pneumonia. Systematic pathogen testing included cultures, serology, urine antigen tests, and molecular detection. Accuracy of procalcitonin to discriminate between viral and bacterial pathogens was calculated.
Results.
Among 1735 patients, pathogens were identified in 645 (37%), including 169 (10%) with typical bacteria, 67 (4%) with atypical bacteria, and 409 (24%) with viruses only. Median procalcitonin concentration was lower with viral pathogens (0.09 ng/mL; interquartile range [IQR], less than 0.05–0.54 ng/mL) than atypical bacteria (0.20 ng/mL; IQR, less than 0.05–0.87 ng/mL; P = .05), and typical bacteria (2.5 ng/mL; IQR, 0.29–12.2 ng/mL; P less than .01). Procalcitonin discriminated bacterial pathogens, including typical and atypical bacteria, from viral pathogens with an area under the receiver operating characteristic (ROC) curve of 0.73 (95% confidence interval [CI], .69–.77). A procalcitonin threshold of 0.1 ng/mL resulted in 80.9% (95% CI, 75.3%–85.7%) sensitivity and 51.6% (95% CI, 46.6%–56.5%) specificity for identification of any bacterial pathogen. Procalcitonin discriminated between typical bacteria and the combined group of viruses and atypical bacteria with an area under the ROC curve of 0.79 (95% CI, .75–.82).
Conclusions.
No procalcitonin threshold perfectly discriminated between viral and bacterial pathogens, but higher procalcitonin strongly correlated with increased probability of bacterial pathogens, particularly typical bacteria.
Renin-aldosterone profiling for all hypertensives? Have we come full circle?
Decades ago John Laragh popularized renin
profiling for the evaluation of hypertensive patients. But due to
limited availability of
testing in community practice and a shift in the way population based
research was applied to the treatment of hypertension it fell out of
favor. More recently interest has resurfaced. In a recent issue of
JACC there is a paper
on the prevalence and clinical characteristics of primary
aldosteronism. From the paper:
Background Despite being widely recognized as the most common form of secondary hypertension, among the general hypertensive population the true prevalence of primary aldosteronism (PA) and its main subtypes, aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), remains a matter of debate.
Objectives This study sought to determine the prevalence and clinical phenotype of PA in a large cohort of unselected patients with hypertension, consecutively referred to our hypertension unit, by 19 general practitioners from Torino, Italy.
Methods Following withdrawal from all interfering medications, patients were screened for PA using the ratio of serum aldosterone to plasma renin activity. PA was diagnosed according to Endocrine Society guidelines. The diagnosis was confirmed or excluded by an intravenous saline infusion test or captopril challenge test and subtype differentiation was performed by adrenal computed tomography scanning and adrenal vein sampling, using strict criteria to define successful cannulation and lateralization of aldosterone production.
Results A total of 1,672 primary care patients with hypertension (569 newly diagnosed and 1,103 patients already diagnosed with arterial hypertension) were included in the study. A total of 99 patients (5.9%) were diagnosed with PA and conclusive subtype differentiation by adrenal vein sampling was made in 91 patients (27 patients with an APA and 64 patients with BAH). The overall prevalence of PA increased with the severity of hypertension, from 3.9% in stage 1 hypertension to 11.8% in stage 3 hypertension. Patients with PA more frequently displayed target organ damage and cardiovascular events compared with those without PA, independent of confounding variables.
Conclusions Our results demonstrated that PA is a frequent cause of secondary hypertension, even in the general population of patients with hypertension, and indicates that most of these patients should be screened for PA.
An
editorial in the
same issue advocates for screening of all hypertensives.
There were some eye opening findings. Of the target organ
complications cited above, LVH was seen in 54% of patients with PA vs
32% of those with essential hypertension (EH), microalbuminuria in
27% with PA vs 13% with EH and cardiovascular events in 15% with PA
vs 6% with EH. Serum potassium was not a useful marker, as
hypokalemia was seen in only 29% of those with PA.
Screening is not that difficult but what if the patient tests
positive? That would lead to a lot of CT scans and invasive adrenal
vein samplings. As the speaker in the audio file said, it’s
something to think about the next time a patient with hypertension
comes into your office.
PPI use may be associated with better heart failure outcomes
Abstract
Background It has been recently reported that histamine H2 receptor antagonists (H2RAs) are associated with impairment of ventricular remodeling and incident heart failure. In addition, favorable pleiotropic effects and adverse effects of proton pump inhibitors (PPIs) on cardiovascular disease have also been reported. We examined the associations of acid suppressive therapy using H2RAs or PPIs with cardiac mortality in patients with heart failure.
Methods and Results In total, 1191 consecutive heart failure patients were divided into 3 groups: a non–acid suppressive therapy group (n=363), an H2RA group (n=164), and a PPI group (n=664). In the follow‐up period (mean 995 days), 169 cardiac deaths occurred. In the Kaplan–Meier analysis, cardiac mortality was significantly lower in the PPI group than in the H2RA and non–acid suppressive therapy groups (11.0% versus 21.3% and 16.8%, respectively; log‐rank P=0.004). In the multivariable Cox proportional hazards analysis, use of PPIs, but not H2RAs, was found to be an independent predictor of cardiac mortality (PPIs: hazard ratio 0.488, P=0.002; H2RAs: hazard ratio 0.855, P=0.579). The propensity‐matched 1:1 cohort was assessed based on propensity score (H2RAs, n=164; PPIs, n=164). Cardiac mortality was significantly lower in the PPI group than in the H2RA group in the postmatched cohort (log‐rank P=0.025). In the Cox proportional hazards analysis, the use of PPIs was a predictor of cardiac mortality in the postmatched cohort (hazard ratio 0.528, P=0.028).
Conclusions PPIs may
be associated with better outcome in patients with heart failure.
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