Saturday, September 23, 2017

Risk of thrombosis in patients with essential thrombocythemia



Abstract

To assess the role of platelet (PLT) count for thrombotic complications in Essential Thrombocythemia (ET), 1201 patients followed in 11 Hematological centers in the Latium region were retrospectively evaluated. At multivariate analysis, the following factors at diagnosis were predictive for a worse Thrombosis-free Survival (TFS): the occurrence of previous thrombotic events (p = 0.0004), age greater than  60 years (p = 0.0044), spleen enlargement (p = 0.042) and a lower PLT count (p = 0.03). Receiver Operating Characteristic (ROC) analyses based on thrombotic events during follow-up identified a baseline platelet count of 944 × 109/l as the best predictive threshold: thrombotic events were 40/384 (10.4%) in patients with PLT count greater than 944 × 109/l and 109/817 (13.3%) in patients with PLT count less than 944 × 109/l, respectively (p = 0.04). Patients with PLT count less than 944 × 109/l were older (median age 60.4 years. vs 57.1 years., p = 0.016), had a lower median WBC count (8.8 × 109/l vs 10.6 × 109/l, p less than 0.0001), a higher median Hb level (14.1 g/dl vs 13.6 g/dl, p less than 0.0001) and a higher rate of JAK-2-V617F positivity (67.2% vs 41.6%, p less than 0.0001); no difference was observed as to thrombotic events before diagnosis, spleen enlargement and concomitant Cardiovascular Risk Factors. In conclusion, our results confirm the protective role for thrombosis of an high PLT count at diagnosis. The older age and the higher rate of JAK-2 V617F positivity in the group of patients with a baseline lower PLT count could in part be responsible of this counterintuitive finding.

The last sentence helps explain the paradox.

Friday, September 22, 2017

Adult onset Still’s disease


Thursday, September 21, 2017

Epinephrine in cardiac arrest: how strongly is it supported by the evidence?



Background

Sudden cardiac arrest accounts for approximately 15% of deaths in developed nations, with poor survival rate. The American Heart Association states that epinephrine is reasonable for patients with cardiac arrest, though the literature behind its use is not strong.

Objective

To review the evidence behind epinephrine for cardiac arrest.

Discussion

Sudden cardiac arrest causes over 450,000 deaths annually in the United States. The American Heart Association recommends epinephrine may be reasonable in patients with cardiac arrest, as part of Advanced Cardiac Life Support. This recommendation is partly based on studies conducted on dogs in the 1960s. High-dose epinephrine is harmful and is not recommended. Epinephrine may improve return of spontaneous circulation, but does not improve survival to discharge or neurologic outcome. Literature suggests that three phases of resuscitation are present: electrical, circulatory, and metabolic. Epinephrine may improve outcomes in the circulatory phase prior to 10 min post arrest, though further study is needed. Basic Life Support measures including adequate chest compressions and early defibrillation provide the greatest benefit.

Conclusions

Epinephrine may improve return of spontaneous circulation, but it does not improve survival to discharge or neurologic outcome. Timing of epinephrine may affect patient outcome, but Basic Life Support measures are the most important aspect of resuscitation and patient survival.


Wednesday, September 20, 2017

EMRs slow physicians down and distract from real clinical care


Tuesday, September 19, 2017

An automated warning system for deteriorating ward patients modestly improved outcomes




Background

Delayed response to clinical deterioration of ward patients is common.

Methods

We performed a prospective before-and-after study in all patients admitted to two clinical ward areas in a district general hospital in the UK. We examined the effect on clinical outcomes of deploying an electronic automated advisory vital signs monitoring and notification system, which relayed abnormal vital signs to a rapid response team (RRT).

Results

We studied 2139 patients before (control) and 2263 after the intervention. During the intervention the number of RRT notifications increased from 405 to 524 (p = 0.001) with more notifications triggering fluid therapy, bronchodilators and antibiotics. Moreover, despite an increase in the number of patients with “do not attempt resuscitation” orders (from 99 to 135; p = 0.047), mortality decreased from 173 to 147 (p = 0.042) patients and cardiac arrests decreased from 14 to 2 events (p = 0.002). Finally, the severity of illness in patients admitted to the ICU was reduced (mean Acute Physiology and Chronic Health Evaluation II score: 26 (SD 9) vs. 18 (SD 8)), as was their mortality (from 45% to 24%; p = 0.04).

Conclusions

Deployment of an electronic automated advisory vital signs monitoring and notification system to signal clinical deterioration in ward patients was associated with significant improvements in key patient-centered clinical outcomes.

This sort of thing has great potential if usage is optimized. Unfortunately, RRT usage has gone far beyond the original intent and unintended consequences abound.


Monday, September 18, 2017

Risk factors for atrial fibrillation in the elderly


Comprehensive free full text review.

Sunday, September 17, 2017

A pleural effusion may have more than one etiology


---especially given recent trends toward increasingly frequent complex comorbidities. From a recent review:

Abstract:

Purpose of review: Historically, pleural effusions have been attributed to a single cause. There is growing recognition that a substantial proportion of pleural effusions may have more than one underlying cause. The purpose of this review is to summarise recent findings regarding the diagnosis and treatment of effusions secondary to more than one aetiology.

Recent findings: A recent prospective study identified that 30% of pleural effusions had more than one underlying aetiology. With a rising prevalence of cardiovascular and malignant disease, the incidence of the complex pleural patient is increasing. The use of biomarkers, including pro-B-type natriuretic peptide, have been suggested as a way of identifying contributing disease process.

Summary: Understanding that there are potentially concurrent causes to a pleural effusion is vital in establishing the diagnoses of multiple underlying aetiologies. New diagnostic pathways, with increasing use of biomarkers, will be required to identify the complex pleural effusion. Further studies on whether the targeting of separate aetiologies improves outcomes will help develop future management strategies.

Saturday, September 16, 2017

DOAC dosing errors



Three points to be made here:

DOAC dosing is much more “indication based” than warfarin.

DOAC may be less forgiving of dosing errors than warfarin.

Unlike warfarin, DOACs have no monitoring safety net.

Friday, September 15, 2017

Thursday, September 14, 2017

Are blood ammonia levels helpful?



Here are their recommendations:

HE is a diagnosis of exclusion and is made on clinical grounds.

Do not check serum ammonia levels in patients with CLD to diagnose HE, to assess the severity of HE, or to determine whether HE is resolving.

Use your clinical evaluation to determine the severity and course of HE.

Treatment should be tailored according to clinical findings, not ammonia levels.

I get a little nervous about absolute recommendations to stop a widely accepted, physiologically rational, low tech, low harm practice just because there’s a lack of “high level” supporting evidence. An unfounded assumption here is that a lack of high level evidence equates to evidence against.

Another questionable assumption is that the test inherently is bad. Certainly at the cutoff of 55, as cited in the article, the test characteristics are poor. At extreme values, however, it may be more helpful. In a comatose patient presenting to ER whose baseline level is known to be 40, for example, a triple digit ammonia may add greatly to the diagnostic confidence and obviate an MRI and LP pending a therapeutic trial directed at HE. In such a case it might even save resources. This article strikes me as a case of black and white thinking. How about a more nuanced approach in which the ordering threshold is proportional to the cost and potential harm of the test?

Wednesday, September 13, 2017

Benzos and opiates given to ward patients increase the risk of deterioration (ICU transfer or arrest)




BACKGROUND

Opioids and benzodiazepines are frequently used in hospitals, but little is known about outcomes among ward patients receiving these medications.

OBJECTIVE

To determine the association between opioid and benzodiazepine administration and clinical deterioration.

DESIGN

Observational cohort study.

SETTING

500-bed academic urban tertiary-care hospital.

PATIENTS

All adults hospitalized on the wards from November 2008 to January 2016 were included. Patients who were “comfort care” status, had tracheostomies, sickle-cell disease, and patients at risk for alcohol withdrawal or seizures were excluded.

MEASUREMENTS

The primary outcome was the composite of intensive care unit transfer or ward cardiac arrest. Discrete-time survival analysis was used to calculate the odds of this outcome during exposed time periods compared to unexposed time periods with respect to the medications of interest, with adjustment for patient demographics, comorbidities, severity of illness, and pain score.

RESULTS

In total, 120,518 admissions from 67,097 patients were included, with 67% of admissions involving opioids, and 21% involving benzodiazepines. After adjustment, each equivalent of 15 mg oral morphine was associated with a 1.9% increase in the odds of the primary outcome within 6 hours (odds ratio [OR], 1.019; 95% confidence interval [CI], 1.013-1.026; P less than 0.001), and each 1 mg oral lorazepam equivalent was associated with a 29% increase in the odds of the composite outcome within 6 hours (OR, 1.29; CI, 1.16-1.45; P less than 0.001).

CONCLUSION

Among ward patients, opioids were associated with increased risk for clinical deterioration in the 6 hours after administration. Benzodiazepines were associated with even higher risk. These results have implications for ward-monitoring strategies. Journal of Hospital Medicine 2017;12:428-434. © 2017 Society of Hospital Medicine


Tuesday, September 12, 2017

Review of the ECG findings in WPW


Monday, September 11, 2017

The ER ECG in drug overdose


Sunday, September 10, 2017

Biomarker guided heart failure treatment versus usual (guideline based) care: take your pick!



Question Does a strategy of titrating therapy to a specific amino-terminal pro–B-type natriuretic peptide (NT-proBNP) target improve clinical outcomes in high-risk patients with heart failure and reduced ejection fraction?

Findings In this randomized clinical trial including 894 adults, a strategy of NT-proBNP–guided therapy compared with usual care did not significantly improve time to first hospitalization or cardiovascular mortality (hazard ratio, 0.98).

Meaning These findings do not support NT-proBNP–guided therapy for management of heart failure with reduced ejection fraction.

From table 2 in the paper we learn that both groups got the same treatment. That is, whether you tended to ignore proBNP levels and just do your best to adhere to guidelines or individualized therapy based on proBNP levels, you ended up with the same regimen. These, or course, were trial participants. What would happen in the real world where guideline goal achievement is horrible?

An accompanying editorial summarized what we knew before:

Assays for natriuretic peptide biomarkers, B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), have become well established for assisting with the diagnosis and assessment of the severity of heart failure and for providing prognostic information in both the setting of acute care of decompensated heart failure and outpatient care of chronic heart failure...

..several randomized clinical trials have evaluated whether the application of serial measurement of natriuretic peptide to guide the titration of medical therapy in chronic heart failure could improve outcomes.4,6 Those trials have yielded mixed results.


Saturday, September 09, 2017

The ECG and future heart failure risk



Background Several markers detected on the routine 12‐lead ECG are associated with future heart failure events. We examined whether these markers are able to separate the risk of heart failure with reduced ejection fraction (HFrEF) from heart failure with preserved ejection fraction (HFpEF).

Methods and Results We analyzed data of 6664 participants (53% female; mean age 62±10 years) from MESA (Multi‐Ethnic Study of Atherosclerosis) who were free of cardiovascular disease at baseline (2000–2002). A competing risks analysis was used to compare the association of several baseline ECG predictors with HFrEF and HFpEF detected during a median follow‐up of 12.1 years. A total of 127 HFrEF and 117 HFpEF events were detected during follow‐up. In a multivariable adjusted model, prolonged QRS duration, delayed intrinsicoid deflection, left‐axis deviation, right‐axis deviation, prolonged QT interval, abnormal QRS‐T axis, left ventricular hypertrophy, ST/T‐wave abnormalities, and left bundle‐branch block were associated with HFrEF. In contrast, higher resting heart rate, abnormal P‐wave axis, and abnormal QRS‐T axis were associated with HFpEF. The risk of HFrEF versus HFpEF was significantly differently for delayed intrinsicoid deflection (hazard ratio: 4.90 [95% confidence interval (CI), 2.77–8.68] versus 0.94 [95% CI, 0.29–2.97]; comparison P=0.013), prolonged QT interval (hazard ratio: 2.39 [95% CI, 1.55–3.68] versus 0.52 [95% CI, 0.23–1.19]; comparison P less than 0.001), and ST/T‐wave abnormalities (hazard ratio: 2.47 [95% CI, 1.69–3.62] versus 1.13 [95% CI, 0.72–1.77]; comparison P=0.0093).

Conclusions Markers of ventricular repolarization and delayed ventricular activation are able to distinguish between the future risk of HFrEF and HFpEF. These findings suggest a role for ECG markers in the personalized risk assessment of heart failure subtypes.

Friday, September 08, 2017

Glossary of critical appraisal


This piece has some helpful information. However it’s a bit imprecise, offering descriptions that “talk around” the various terms rather than actual definitions.

Wednesday, September 06, 2017

Ace inhibitor use in patients with Duchenne and Becker muscular dystrophy slows progression of myocardial fibrosis



Importance In Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), interventions reducing the progression of myocardial disease could affect survival.

Objective To assess the effect of early angiotensin-converting enzyme (ACE) inhibitor therapy in patients with normal left ventricular function on the progression of myocardial fibrosis (MF) identified on cardiovascular magnetic resonance (CMR).

Design, Setting, and Participants A randomized clinical trial conducted in 2 centers included 76 male patients with DMD or BMD undergoing 2 CMR studies with a 2-year interval for ventricular function and MF assessment. In a non–intent-to-treat trial, 42 patients with MF and normal left ventricular ejection fraction (LVEF) were randomized (1:1) to receive or not receive ACE inhibitor therapy. The study was conducted from June 26, 2009, to June 30, 2012. Data analysis was performed from June 30, 2013, to October 3, 2016.

Interventions Randomization (1:1) to receive or not receive ACE inhibitor therapy.

Main Outcomes and Measures Primary outcome was MF progression from baseline to the 2-year CMR study.

Results Of the 76 male patients included in the study, 70 had DMD (92%) and 6 had BMD (8%); mean (SD) age at baseline was 13.1 (4.4) years. Myocardial fibrosis was present in 55 patients (72%) and LV systolic dysfunction was identified in 13 patients (24%). Myocardial fibrosis at baseline was an independent indicator of lower LVEF at follow-up (coefficient [SE], −0.16 [0.07]; P = .03). Among patients with MF and preserved LVEF (42 [55%]), those randomized (21 patients in each arm) to receive ACE inhibitors demonstrated slower MF progression compared with the untreated group (mean [SD] increase of 3.1% [7.4%] vs 10.0% [6.2%] as a percentage of LV mass; P = .001). In multivariate analysis, ACE inhibitor therapy was an independent indicator of decreased MF progression (coefficient [SE], −4.51 [2.11]; P = .04). Patients with MF noted on CMR had a higher probability of cardiovascular events (event rate, 10 of 55 [18.2%] vs 0 of 21 [0%]; log-rank P = .04).

Conclusions and Relevance In this 2-year, follow-up, randomized clinical trial of patients with Duchenne or Becker muscular dystrophy whose LVEF was preserved and MF was present as determined on CMR, ACE inhibitor therapy was associated with significantly slower progression of MF. The presence of MF was associated with worse patient prognosis.


Tuesday, September 05, 2017

Sunday, September 03, 2017

DM 2 as a part of post intensive care syndrome



Here’s a paradox from the text of the paper that caught my notice:

Teleologically, IR is considered an evolutionary preserved mechanism designed to supply higher amounts of glucose to insulin-independent tissues than to insulin-dependent tissues [2].

Friday, September 01, 2017

What should you do with distal DVT?


From a recent review:


Distal (or calf) DVT is a very common medical condition, representing half of all diagnosed DVTs.

The diagnostic performances of venous compression ultrasound are lower for the diagnosis of distal DVT compared to proximal DVT.

All patients with distal DVT do not necessarily require anticoagulant treatment.

Low-risk outpatients may benefit from ultrasound surveillance alone, without any anticoagulation.

In high-risk patients, such as inpatients, patients with cancer or previous DVT, therapeutic anticoagulation is recommended.

Thursday, August 31, 2017

Digoxin use for atrial fibrillation and mortality



Methods and Results In the ENGAGE AF‐TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation‐Thrombolysis in Myocardial Infarction 48) trial, clinical outcomes of patients with atrial fibrillation with and without HF were examined by baseline digoxin use during a median follow‐up of 2.8 years. HF was defined at baseline as prior or current clinical stage C or D HF. Of 21 105 patients enrolled, 6327 (30%) were treated with digoxin at baseline. Among patients without HF (n=8981), digoxin use (20%) was independently associated with sudden cardiac death (adjusted hazard ratio, 1.51; 95% CI, 1.10–2.08), with no significant interaction by age, sex, left ventricular ejection fraction, renal function, or concomitant medications (P greater than 0.05 for each). Consistent results were observed using propensity matching (adjusted hazard ratio for sudden cardiac death, 1.90; 95% CI, 1.36–2.65). Among patients with HF (n=12 124), digoxin use (37%) was associated with an increase in all‐cause death, cardiovascular death, sudden cardiac death, and death caused by HF/cardiogenic shock (P less than 0.01 for each), but not with noncardiovascular death, stroke/systemic embolism, or myocardial infarction.

Conclusions In this observational analysis of patients with atrial fibrillation without investigator‐reported HF, digoxin use was significantly associated with sudden cardiac death. While residual confounding cannot be excluded, the association between digoxin use and worse clinical outcomes highlights the need to examine digoxin use, particularly when prescribed to control heart rate in patients with atrial fibrillation in a randomized trial.

Tuesday, August 29, 2017

DIC in sepsis


Here are some key points from a recent review. The review is available as free full text.

DIC is characterized by activation of procoagulant factors (with an important role of tissue factor expression from activated monocytes and endothelial cells) and down regulation of natural anticoagulants and fibrinolytics (protein C, plasminogen activator and others).

Thus, while clotting may dominate the picture early on clotting factors are consumed, moving the picture toward the bleeding end of the clinical spectrum. At the point of patient presentation either side of the spectrum may dominate, and often both do.


The spectrum of severity is quite variable.

From the article:

Sepsis is almost invariably associated with coagulation abnormalities. These deviations range from delicate activation of coagulation that can only be identified by highly sensitive assays for coagulation factor activation to somewhat more severe hemostatic activation that may be noticeable by a subtle fall in platelet count and sub-clinical elongation of global clotting assays to fulminant disseminated intravascular coagulation (DIC), manifested by widespread microvascular thrombosis in small and mid-size vessels and simultaneous profuse hemorrhage from various sites [[4], [5]]. Patients with sepsis and extensive forms of DIC may develop overt thrombo-embolic complications or clinically less apparent microvascular clot formation that may contribute to multiple organ failure [[5], [6]]. In other cases, severe hemorrhage may be the dominant presentation [7], and frequently sepsis and DIC leads to simultaneous thrombosis and bleeding. Hemorrhage is due to consumption and subsequent depletion of coagulation factors and platelets, caused by ongoing activation of the hemostatic system [8]. In its most extreme manifestation this combination may present as the Waterhouse-Friderichsen syndrome, typically observed during fulminant meningococcal septicemia, although many other microorganisms may cause this clinical situation as well [9].


How often is sepsis accompanied by DIC?

Some degree of coagulation disturbance is present in virtually all patients but it may be subclinical. According to the article 50-70% of patients will have clinically relevant coagulation changes and about 35% will meet criteria for DIC. (Published criteria for overt DIC and non overt DIC are based on scoring systems and are found here).


A drop in platelets occurs in almost all patients with sepsis and the mechanisms are multiple and complex.

From the article:

The vast majority of patients with sepsis will develop thrombocytopenia (platelet count less than 150 × 109/l) [[11], [12]]. Commonly, platelet count drops in the first four days following admission to the hospital [13]. The severity of sepsis correlates strongly with the decrease in platelet count [14]. Crucial factors that cause thrombocytopenia in sepsis are decreased platelet production, enhanced consumption, obliteration, or sequestration in the spleen. Impaired production of megakaryocytes in the bone marrow may seem incongruous with the high levels of platelet production-stimulating pro-inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, and elevated levels of thrombopoietin in patients with sepsis, which theoretically should stimulate megakaryopoiesis [15]. However, in a large number of patients with sepsis substantial hemophagocytosis occurs, consisting of active phagocytosis of platelet precursors and other hematopoietic cells by mononuclear cells, presumably caused by elevated concentrations of macrophage colony stimulating factor (M-CSF) in sepsis [16]. Platelet consumption is presumably also important in sepsis, due to platelet activation secondary to continuous formation of thrombin.


Monday, August 28, 2017

Desmopressin spray approved for nocturnal polyuria


Sunday, August 27, 2017

Follow up ultrasound and D dimer testing to help guide the duration of anticoagulation for DVT



Abstract

Background

The optimal long-term strategy for preventing recurrent venous thromboembolism (VTE) in patients with deep-vein thrombosis (DVT) is uncertain.
Methods

In 620 consecutive outpatients with a first proximal DVT who had completed at least three months of anticoagulation (unprovoked in 483, associated with minor risk factors in 137), the ultrasound presence of residual vein thrombosis (RVT) was assessed and defined as an incompressibility of at least 4 mm. In 517 patients without RVT and with negative D-dimer, anticoagulation was stopped and D-dimer was repeated after one and three months. Anticoagulation was resumed in 63 of the 72 patients in whom D-dimer reverted to positivity.

Results

During a mean follow-up of three years, recurrent VTE developed in 40 (7.7%) of the 517 patients, leading to an annual rate of 3.6% (95% CI, 2.6 to 4.9): 4.1% (95% CI, 2.9 to 5.7) in individuals with unprovoked DVT, and 2.2% (95% CI, 1.1 to 4.5) in those with DVT associated with minor risk factors. Of the 233 males with unprovoked DVT, 17 (7.3%) developed events in the first year of follow-up. Major bleeding complications occurred in 8 patients while on anticoagulation, leading to an annual rate of 1.2% (95% CI, 0.6 to 2.4).

Conclusions

Discontinuing anticoagulation in patients with a first episode of proximal DVT based on the assessment of RVT and serial D-dimer leads to an overall annual rate of recurrent VTE lower than 5.0%, which is the rate deemed as acceptable by the Subcommittee on Control of Anticoagulation of the ISTH. However, in males with unprovoked DVT there is room for further improving the long-term strategy of VTE prevention.

The current Chest guidelines raise similar concerns about men and recommend against the use of D dimer guidance in men.




Monday, August 14, 2017

When can one discontinue non invasive positive pressure ventilation in severe COPD exacerbation?



Abstract

We assessed whether prolongation of nocturnal noninvasive ventilation (NIV) after recovery from acute hypercapnic respiratory failure (AHRF) in chronic obstructive pulmonary disease (COPD) patients with NIV could prevent subsequent relapse of AHRF.

A randomised controlled trial was performed in 120 COPD patients without previous domiciliary ventilation, admitted for AHRF and treated with NIV. When the episode was resolved and patients tolerated unassisted breathing for 4 h, they were randomly allocated to receive three additional nights of NIV (n=61) or direct NIV discontinuation (n=59). The primary outcome was relapse of AHRF within 8 days after NIV discontinuation.

Except for a shorter median (interquartile range) intermediate respiratory care unit (IRCU) stay in the direct discontinuation group (4 (2–6) versus 5 (4–7) days, p=0.036), no differences were observed in relapse of AHRF after NIV discontinuation (10 (17%) versus 8 (13%) for the direct discontinuation and nocturnal NIV groups, respectively, p=0.56), long-term ventilator dependence, hospital stay, and 6-month hospital readmission or survival.

Prolongation of nocturnal NIV after recovery from an AHRF episode does not prevent subsequent relapse of AHRF in COPD patients without previous domiciliary ventilation, and results in longer IRCU stay. Consequently, NIV can be directly discontinued when the episode is resolved and patients tolerate unassisted breathing.


NIV can be directly discontinued when a COPD exacerbation is resolved and patients tolerate unassisted breathing

Thursday, August 10, 2017

Atrial fibrillation onset in ICU patients





Objective: To determine the association of new-onset atrial fibrillation with outcomes, including ICU length of stay and survival.

Design: Retrospective cohort of ICU admissions. We found atrial fibrillation using automated detection (greater than or equal to 90 s in 30 min) and classed as new-onset if there was no prior diagnosis of atrial fibrillation. We identified determinants of new-onset atrial fibrillation and, using propensity matching, characterized its impact on outcomes.

Setting: Tertiary care academic center.

Patients: A total of 8,356 consecutive adult admissions to either the medical or surgical/trauma/burn ICU with available continuous electrocardiogram data.

Interventions: None.

Measurements and Main Results: From 74 patient-years of every 15-minute observations, we detected atrial fibrillation in 1,610 admissions (19%), with median burden less than 2%. Most atrial fibrillation was paroxysmal; less than 2% of admissions were always in atrial fibrillation. New-onset atrial fibrillation was subclinical or went undocumented in 626, or 8% of all ICU admissions. Advanced age, acute respiratory failure, and sepsis were the strongest predictors of new-onset atrial fibrillation. In propensity-adjusted regression analyses, clinical new-onset atrial fibrillation was associated with increased hospital mortality (odds ratio, 1.63; 95% CI, 1.01–2.63) and longer length of stay (2.25 d; CI, 0.58–3.92). New-onset atrial fibrillation was not associated with survival after hospital discharge (hazard ratio, 0.99; 95% CI, 0.76–1.28 and hazard ratio, 1.11; 95% CI, 0.67–1.83, respectively, for subclinical and clinical new-onset atrial fibrillation).

Conclusions: Automated analysis of continuous electrocardiogram heart rate dynamics detects new-onset atrial fibrillation in many ICU patients. Though often transient and frequently unrecognized, new-onset atrial fibrillation is associated with poor hospital outcomes.

Tuesday, August 01, 2017

Antibiotic associated adverse events in hospitalized patients



Importance Estimates of the incidence of overall antibiotic-associated adverse drug events (ADEs) in hospitalized patients are generally unavailable.

Objective To describe the incidence of antibiotic-associated ADEs for adult inpatients receiving systemic antibiotic therapy.

Design, Setting, and Participants Retrospective cohort of adult inpatients admitted to general medicine wards at an academic medical center.

Exposures At least 24 hours of any parenteral or oral antibiotic therapy.

Main Outcomes and Measures Medical records of 1488 patients were examined for 30 days after antibiotic initiation for the development of the following antibiotic-associated ADEs: gastrointestinal, dermatologic, musculoskeletal, hematologic, hepatobiliary, renal, cardiac, and neurologic; and 90 days for the development of Clostridium difficile infection or incident multidrug-resistant organism infection, based on adjudication by 2 infectious diseases trained clinicians.

Results In 1488 patients, the median age was 59 years (interquartile range, 49-69 years), and 758 (51%) participants were female. A total of 298 (20%) patients experienced at least 1 antibiotic-associated ADE. Furthermore, 56 (20%) non–clinically indicated antibiotic regimens were associated with an ADE, including 7 cases of C difficile infection. Every additional 10 days of antibiotic therapy conferred a 3% increased risk of an ADE. The most common ADEs were gastrointestinal, renal, and hematologic abnormalities, accounting for 78 (42%), 45 (24%), and 28 (15%) 30-day ADEs, respectively. Notable differences were identified between the incidence of ADEs associated with specific antibiotics.

Conclusions and Relevance Although antibiotics may play a critical role when used appropriately, our findings underscore the importance of judicious antibiotic prescribing to reduce the harm that can result from antibiotic-associated ADEs.


Monday, July 31, 2017

Timing of anticoagulant initiation for atrial fibrillation in patients with intracerebral hemorrhage



Background and Purpose—This study aims to provide observational data on the relationship between the timing of antithrombotic treatment and the competing risks of severe thrombotic and hemorrhagic events in a cohort of Swedish patients with atrial fibrillation and intracerebral hemorrhage (ICH).

Methods—Patients with atrial fibrillation and a first-ever ICH were identified in the Swedish Stroke Register, Riksstroke, 2005 to 2012. Riksstroke was linked with other national registers to find information on treatment, comorbidity, and outcome. The optimal timing of treatment in patients with low and high thromboembolic risk was described through cumulative incidence functions separately for thrombotic and hemorrhagic events and for the combined end point vascular death or nonfatal stroke.

Results—The study included 2619 ICH survivors with atrial fibrillation with 5759 person-years of follow-up. Anticoagulant treatment was associated with a reduced risk of vascular death and nonfatal stroke in high-risk patients with no significantly increased risk of severe hemorrhage. The benefit seemed to be greatest when treatment was started 7 to 8 weeks after ICH. For high-risk women, the total risk of vascular death or stroke recurrence within 3 years was 17.0% when anticoagulant treatment was initiated 8 weeks after ICH and 28.6% without any antithrombotic treatment (95% confidence interval for difference, 1.4%–21.8%). For high-risk men, the corresponding risks were 14.3% versus 23.6% (95% confidence interval for difference, 0.4%–18.2%).

Conclusions—This nationwide observational study suggests that anticoagulant treatment may be initiated 7 to 8 weeks after ICH in patients with atrial fibrillation to optimize the benefit from treatment and minimize risk.