Wednesday, January 30, 2019
Some interesting questions were asked. For example, is lactate an indicator of tissue oxygenation in sepsis? Evidence suggests it may be due to a metabolic effect instead, unrelated to tissue hypoxia, that is, type b lactic acidosis. Nevertheless it appears to be a useful marker to follow. Certainly its elevation portends a worse outcome but maybe not by the mechanism we think. See here. All this is not to say that type a lactic acidosis does not exist (that is, is not due to tissue ischemia in other forms of shock, in low cardiac output states or in high demand states).
How strong is the evidence in favor of fluid resuscitation in sepsis? Pretty weak. The author talks around the idea, but comes short, of saying we should stop doing it. He also talks around the idea, but comes just short, of saying there is equipoise for a controlled trial of fluid resuscitation versus no fluid resuscitation.
From a recent review:
Short telomere syndromes (STSs) are accelerated aging syndromes with multisystemic manifestations that present complex management challenges. In this article, we discuss a single-institution experience in diagnosing and managing patients with inherited STSs. In total, we identified 17 patients with short telomeres, defined by flow-fluorescence in-situ hybridization telomere lengths of less than first centile in granulocytes/lymphocytes OR the presence of a characteristic germline pathogenic variant in the context of a highly suggestive clinical phenotype. Genetic variations in the telomere complex were identified in 6 (35%) patients, with 4 being known pathogenic variants involving TERT (n=2), TERC (n=1), and DKC1 (n=1) genes, while 2 were variants of uncertain significance in TERT and RTEL1 genes. Idiopathic interstitial pneumonia (IIP) (n=12 [71%]), unexplained cytopenias (n=5 [29%]), and cirrhosis (n=2 [12%]) were most frequent clinical phenotypes at diagnosis. At median follow-up of 48 (range, 0-316) months, Kaplan-Meier estimate of overall survival, median (95% CI), was 182 (113, not reached) months. Treatment modalities included lung transplantation for IIP (n=5 [29%]), with 3 patients developing signs of acute cellular rejection (2, grade A2; 1, grade A1); danazol therapy for cytopenias (n=4 [24%]), with only 1 out of 4 patients showing a partial hematologic response; and allogeneic hematopoietic stem cell transplant for progressive bone marrow failure (n=2), with 1 patient dying from transplant-related complications. In summary, patients with STSs present with diverse clinical manifestations and require a multidisciplinary approach to management, with organ-specific transplantation capable of providing clinical benefit.
Tuesday, January 29, 2019
Methods: Eligible patients were fee-for-service Medicare beneficiaries 65 years and older hospitalized at an acute-care hospital for AMI between 2011 and 2014. Spending was defined as hospital-level risk-standardized payments associated with a 30-day episode of AMI care, stratified into low ( less than 25 percentile), average (greater than or equal to 25 to less than or equal to 75 percentile), and high (greater than 75 percentile) spending groups. The primary outcome was mortality within 30 days of admission. To examine the association between hospital-level 30-day spending and mortality, we fitted mixed-effects logistic regression models with random hospital intercepts to model 30-day mortality as a function of patients’ admitting hospital’s expenditure.
Results: We included 642,105 index hospitalizations for AMI at 2,319 acute-care hospitals. Hospitals with higher 30-day spending were larger, tended to be teaching hospitals, were more often located in an urban area, were more likely to have cardiac catheterization laboratories and cardiac surgery capability, and also had higher rates of coronary revascularization. Across hospital groups, median 30-day spending per beneficiary was $20,207 (low), $22,018 (average), and $24,174 (high). Higher hospital-level 30-day spending was associated with lower 30-day mortality even after adjustment for patient and hospital characteristics (adjusted odds ratio for additional $1000 spending, 0.989; 95% confidence interval 0.982-0.996, p=0.002). This relationship was not attenuated following additional adjustment for hospital-level revascularization rates.
Monday, January 28, 2019
A new suspected cause of cryptic strokes is “silent atrial fibrillation.” Pacemakers and other implanted devices allow continuous recording of cardiac rhythm for months or years. They have discovered that short periods of atrial fibrillation lasting minutes or hours are frequent and usually are asymptomatic. A meta-analysis of 50 studies involving more than 10,000 patients with a recent stroke found that 7.7% had new atrial fibrillation on their admitting electrocardiogram. In 3 weeks during and after hospitalization, another 16.9% were diagnosed. A total of 23.7% of these stroke patients had silent atrial fibrillation; that is, atrial fibrillation diagnosed after hospital admission. Silent atrial fibrillation is also frequent in patients with pacemakers who do not have a recent stroke. In a pooled analysis of 3 studies involving more than 10,000 patients monitored for 24 months, 43% had at least 1 day with atrial fibrillation lasting more than 5 minutes. Ten percent had atrial fibrillation lasting at least 12 hours. Despite the frequency of silent atrial fibrillation in these patients with multiple risk factors for stroke, the annual incidence of stroke was only 0.23%. When silent atrial fibrillation is detected in patients with recent cryptogenic stroke, anticoagulation is indicated. In patients without stroke, silent atrial fibrillation should lead to further monitoring for clinical atrial fibrillation rather than immediate anticoagulation, as some have advocated.
These can take the form of extraintestinal manifestations of the IBD itself or disease associations due to shared risk factors.
They can occur in both ulcerative colitis and Crohn disease.
Direct extraintestinal manifestations include bronchiolitis, obliterative bronchiolitis and bronchiectasis.
Associated diseases include asthma and sarcoidosis.
Sunday, January 27, 2019
Radioactive iodine therapy and antithyroid medications produce similar health-related quality-of-life outcomes in patients with Graves disease. Radioactive iodine therapy is an appropriate choice for patients who prefer definitive treatment. Antithyroid medications are appropriate in patients attempting to avoid long-term thyroid hormone therapy and should be considered in those with increased risk of Graves ophthalmopathy, such as smokers.1 (Strength of Recommendation: B, based on inconsistent or limited-quality patient-oriented evidence.)
Saturday, January 26, 2019
Takotsubo syndrome, also known as stress-induced cardiomyopathy (SC), is underrecognized in cancer patients. This study aims to investigate the incidence, natural history, and triggers of SC in cancer patients and its impact on cancer therapy and overall survival. A total of 30 subjects fulfilled the diagnostic criteria for SC at MD Anderson Cancer Center over a 6-year period. Clinical presentation, electrocardiogram, laboratory data, and transthoracic echocardiogram results registered during the acute phase and follow-up were collected. All patients underwent coronary angiography. The most frequent presenting symptoms were chest pain in 63.3% of the patients and shortness of breath/dyspnea on exertion in 27% of the patients. T-wave inversion was a more common electrocardiographic presentation (60%) than ST elevation (13.3%). The median and interquartile range of peak creatine kinase MB fraction, troponin I, and brain natriuretic peptide were creatine kinase MB fraction 8.9, 4.6 to 21.1; troponin I 1.31, 0.7 to 3.3; and brain natriuretic peptide 1,124, 453.5 to 2,369.5. The most common complication of SC was cardiogenic shock requiring inotropic agents (20%). Of the 21 patients who required ongoing cancer treatment, 16 were able to resume chemotherapy, 5 underwent surgery, and 4 received radiation treatment. Median time to resume cancer treatment was 20 days after SC. None of the patients experienced recurrence of SC and other cardiac events. In conclusion, SC should be considered in the differential diagnosis of cancer patients who present with chest pain and ECG findings characteristic of acute coronary syndrome. Most of these patients normalize ejection fraction and may resume cancer therapy early.
•LMWH is effective in about 60% of LC with PVT patients.•The resolution of thrombus associated with LMWH use is accompanied by improvement in liver function.•It is more effective for PVT treatment to start LMWH early and to maintain it for a long time.•LMWH treatment of usual dose and schedule is tolerable for LC patients.
Portal vein thrombosis (PVT) is a well-known complication in patients with liver cirrhosis (LC). The aim of this study is to investigate the outcomes of cirrhotic patients with PVT treated with low-molecular-weight heparin (LMWH).
Ninety-one LC patients with PVT were treated with dalteparin or enoxaparin for six months. Patients with major bleeding during the last three months, severe thrombocytopenia, or impaired renal function were excluded.
The median age was 62.9 years, and 59 patients had hepatocellular carcinoma. The overall recanalization rate was 61.5%. Patients with a favorable Child-Pugh class and those recently diagnosed as having a thrombus showed significantly better responses. In those who responded to the anticoagulation therapy, the post-treatment bilirubin and platelet levels were improved compared to those in the pre-treatment state. The relapse rate for PVT was 56.6%, and the median time to relapse was 4.0 months. Bleeding was reported in 13 patients (14.4%), and two patients died due to fatal bleeding. A history of variceal bleeding and low serum albumin were risk factors for bleeding.
LMWH therapy for PVT in LC is effective. Advanced LC and a delayed start of anticoagulation treatment decrease the effect of LMWH. Despite its effectiveness, there is a risk of hemorrhage, hence anticoagulation should be carefully considered, especially in patients with advanced LC and a history of variceal bleeding.
Friday, January 25, 2019
Peter Pronovost, a champion of this sort of thing, along with a couple of other authors, cites weaknesses of public reporting, correctly pointing out that when hospitals do it themselves it’s largely just self promotional. Their solution? Beef up the standards by getting outside organizations like CMS and Leapfrog involved. Seriously? They’ve been at this for years with little evidence that patients are really interested, let alone helped.
The definition of sepsis is a mess. Sepsis is difficult to reduce to a set of criteria. If you are an experienced clinician you know it when you see it. This is just one reason why the CMS measure is a disaster.
From the linked article:
In changing the clinically significant value of lactate, CMS mandated that clinical practice, hospital protocols, and medical education had to adopt the lower threshold of 2 mmol/L to define severe sepsis and an initial lactate of greater than 4 mmol/L to define septic shock in the absence of robust supportive literature. Physicians are being forced to use government-issued standards of practice and patient care that have not been fully investigated as appropriate and safe. Doctors are no longer permitted to doctor but rather forced to practice cookie cutter one-size-fits-all algorithms with regard to sepsis care. These constraints leave the clinician in the predicament of using best practices versus following mandated guidelines.
We have demonstrated that there are various proposed definitions for sepsis, severe sepsis and septic shock. This is likely due to the fact that unlike myocardial infarction, which has a very precise pathophysiology and organic effect, sepsis is a spectrum of any number of factors. It is not due to one distinct insult but can be caused by a large variety of infectious agents that can infect a variety of anatomic locations. It is not due to one region of the body suffering hypoxia; rather it is due to a dysregulated host response to infection. And that host response is dependent on a variety of uncontrolled factors such as age, sex and comorbidities. It may be impossible to develop definitions that appropriately identify a disease state that is so dependent on multiple variables. Each patient is different and cannot be defined and treated exactly the same way. The CMS definitions are premature and, unlike the various other definitions presented, are mandatory and must be followed by clinicians practicing in the United States.
Why not let doctors be doctors? Because there is so much variation, of course. And as we all know variation is the enemy, right?
Here is a report on hospitals’ perceptions of SEP-1:
BACKGROUND: In October 2015, the Centers for Medicare and Medicaid Services (CMS) implemented the Sepsis CMS Core Measure (SEP-1) program, requiring hospitals to report data on the quality of care for their patients with sepsis.
OBJECTIVE: We sought to understand hospital perceptions of and responses to the SEP-1 program.
DESIGN: A thematic content analysis of semistructured interviews with hospital quality officials.
SETTING: A stratified random sample of short-stay, nonfederal, general acute care hospitals in the United States.
SUBJECTS: Hospital quality officers, including nurses and physicians.
MEASUREMENTS: We completed 29 interviews before reaching content saturation.
RESULTS: Hospitals reported a variety of actions in response to SEP-1, including new efforts to collect data, improve sepsis diagnosis and treatment, and manage clinicians’ attitudes toward SEP-1. These efforts frequently required dedicated resources to meet the program’s requirements for treatment and documentation, which were thought to be complex and not consistently linked to patient-centered outcomes. Most respondents felt that SEP-1 was likely to improve sepsis outcomes. At the same time, they described specific changes that could improve its effectiveness, including allowing hospitals to focus on the treatment processes most directly associated with improved patient outcomes and better aligning the measure’s sepsis definitions with current clinical definitions.
CONCLUSIONS: Hospitals are responding to the SEP-1 program across a number of domains and in ways that consistently require dedicated resources. Hospitals are interested in further revisions to the program to alleviate the burden of the reporting requirements and help them optimize the effectiveness of their investments in quality-improvement efforts.
Saturday, January 19, 2019
Objective: Systemic capillary-leak syndrome is a very rare cause of recurrent hypovolemic shock. Few data are available on its clinical manifestations, laboratory findings, and outcomes of those patients requiring ICU admission. This study was undertaken to describe the clinical pictures and ICU management of severe systemic capillary-leak syndrome episodes.
Design, Setting, Patients: This multicenter retrospective analysis concerned patients entered in the European Clarkson’s disease (EurêClark) Registry and admitted to ICUs between May 1992 and February 2016.
Measurements and Main Results: Fifty-nine attacks occurring in 37 patients (male-to-female sex ratio, 1.05; mean ± SD age, 51 ± 11.4 yr) were included. Among 34 patients (91.9%) with monoclonal immunoglobulin G gammopathy, 20 (58.8%) had kappa light chains. ICU-admission hemoglobin and proteinemia were respectively median (interquartile range) 20.2 g/dL (17.9–22 g/dL) and 50 g/L (36.5–58.5 g/L). IV immunoglobulins were infused (IV immunoglobulin) during 15 episodes (25.4%). A compartment syndrome developed during 12 episodes (20.3%). Eleven (18.6%) in-ICU deaths occurred. Bivariable analyses (the 37 patients’ last episodes) retained Sequential Organ-Failure Assessment score greater than 10 (odds ratio, 12.9 [95% CI, 1.2–140]; p = 0.04) and cumulated fluid-therapy volume greater than 10.7 L (odds ratio, 16.8 [1.6–180]; p = 0.02) as independent predictors of hospital mortality.
Conclusions: We described the largest cohort of severe systemic capillary-leak syndrome flares requiring ICU admission. High-volume fluid therapy was independently associated with poorer outcomes. IV immunoglobulin use was not associated with improved survival; hence, their use should be considered prudently and needs further evaluation in future studies.
Objectives: To determine the association between preadmission oral corticosteroid receipt and the development of acute respiratory distress syndrome in critically ill patients with sepsis.
Design: Retrospective observational study.
Setting: Medical, surgical, trauma, and cardiovascular ICUs of an academic medical center.
Patients: A total of 1,080 critically ill patients with sepsis.
Measurements and Main Results: The unadjusted occurrence rate of acute respiratory distress syndrome within 96 hours of ICU admission was 35% among patients who had received oral corticosteroids compared with 42% among those who had not (p = 0.107). In a multivariable analysis controlling for prespecified confounders, preadmission oral corticosteroids were associated with a lower incidence of acute respiratory distress syndrome in the 96 hours after ICU admission (odds ratio, 0.53; 95% CI, 0.33–0.84; p = 0.008), a finding that persisted in multiple sensitivity analyses. The median daily dose of oral corticosteroids among the 165 patients receiving oral corticosteroids, in prednisone equivalents, was 10 mg (interquartile range, 5–30 mg). Higher doses of preadmission oral corticosteroids were associated with a lower incidence of acute respiratory distress syndrome (odds ratio for 30 mg of prednisone compared with 5 mg 0.53; 95% CI, 0.32–0.86). In multivariable analyses, preadmission oral corticosteroids were not associated with in-hospital mortality (odds ratio, 1.41; 95% CI, 0.87–2.28; p = 0.164), ICU length of stay (odds ratio, 0.90; 95% CI, 0.63–1.30; p = 0.585), or ventilator-free days (odds ratio, 1.06; 95% CI, 0.71–1.57; p = 0.783).
Conclusions: Among ICU patients with sepsis, preadmission oral corticosteroids were independently associated with a lower incidence of early acute respiratory distress syndrome.
Here are some key points from the ATA guidelines:
When TSH is persistently less than 0.1 mU/L, treatment of SH is recommended in all individuals greater than or equal to 65 years of age; in patients with cardiac risk factors, heart disease or osteoporosis; in postmenopausal women who are not on estrogens or bisphosphonates; and in individuals with hyperthyroid symptoms…
When TSH is persistently less than 0.1 mU/L, treatment of SH should be considered in asymptomatic individuals less than 65 years of age without the risk factors listed in Recommendation 73...
When TSH is persistently below the lower limit of normal but greater than or equal to 0.1 mU/L, treatment of SH should be considered in individuals greater than or equal to 65 years of age and in patients with cardiac disease, osteoporosis, or symptoms of hyperthyroidism…
When TSH is persistently below the lower limit of normal but greater than or equal to 0.1 mU/L, asymptomatic patients under age 65 without cardiac disease or osteoporosis can be observed without further investigation of the etiology of the subnormal TSH or treatment.
Friday, January 18, 2019
From the review:
Previously considered rare, SCAD is now recognised to be the cause of 2–4% of all cases of ACS, 24–36% of myocardial infarcts (MI) in women less than 50 years, and the commonest cause of an MI associated with pregnancy. SCAD predominantly affects women (92–98% of cases), who are relatively young (42–52 yrs) and have a low incidence of traditional risk factors.
In addition to primary or isolated SCAD, spontaneous dissection of coronary arteries can occur in association with connective tissue disorders  [e.g., Marfan's syndrome (fibrillin, FBN1, gene defect), Ehlers Danlos, type 4 (collagen, COL3A1, gene), cystic medial necrosis, Loeys-Dietz syndrome (LDS), type II (transforming growth factor B receptor, TGFBR2, or SMAD3 genes); atherosclerotic coronary artery disease; aortic dissection with coronary artery extension, or inflammatory disorders (e.g., systemic lupus erythematosus (SLE), Crohn's disease, ulcerative colitis).
These cases might be termed syndromic (as opposed to primary) SCAD.
More from the review:
There is no single unifying disease process leading to SCAD, although, based on the finding of familial clustering of SCAD cases with involvement of mother-daughter, identical twin sisters, sister-sister, aunt-niece, and first-cousin pairs  , and strong association of SCAD with fibromuscular dysplasia (FMD)…
Risk factors for SCAD include intense physical exercise (isometric or aerobic), Valsalva manoeuvre (e.g., retching, vomiting, bowel movement, coughing), pregnancy (most commonly in the peripartum period)…
Conservative medical management is recommended in patients without ongoing chest pain or ECG changes and usually is associated with spontaneous healing of the affected segment on subsequent angiography  . Long-term aspirin and β-blockers are commonly prescribed, although the rationale for using anti-platelet or anti-coagulant therapy, including aspirin, in patients with an IMH without an intimal tear, is tenuous, given that such therapy may increase bleeding within the vessel wall. Intravenous heparin should not be given or should be stopped in such patients once the diagnosis has been made. Thrombolytic therapy, dual antiplatelet therapy and glycoprotein IIb/IIIa inhibitors should be typically avoided. There is also little rationale for the use of statins unless the patient is dyslipidaemic. Angiotensin converting enzyme inhibitors or angiotensin receptor blockers may be administered to patients with a large MI providing they are not hypotensive.
Percutaneous coronary interventions (PCI) ± stenting should be avoided as outcomes are poor. Moreover, the affected vessel is prone to iatrogenic dissection and extension...
This phenomenon has been known for a long time. This case report highlights the condition and demonstrates the beauty of ladder diagrams.
Thursday, January 17, 2019
Yet another “systems improvement” that has failed to live up to the hype. Sepsis harassment.
Purpose of review
The mechanisms leading to the development of premature atherosclerosis and vascular injury in systemic lupus erythematosus (SLE) remain to be fully elucidated. This is a comprehensive review of recent research developments related to the understanding of cardiovascular disease (CVD) in lupus.
SLE patients with lupus nephritis display significantly increased risk of myocardial infarction and CVD mortality than SLE patients without lupus nephritis. SLE disease-related parameters could be taken into consideration when calculating CVD risks. The type I interferon pathway is detrimental to the vasculature and may contribute to the development of insulin resistance. The level of low-density granulocytes, a distinct subset of proinflammatory neutrophils present in SLE, was independently associated with coronary plaque burden and endothelial dysfunction. Invariant natural killer T cells may promote an atheroprotective effect in SLE patients with asymptomatic atherosclerotic plaques. Oxidized lupus high-density lipoprotein promotes proinflammatory responses in macrophages.
Recent discoveries have further strengthened the critical role of SLE-related immune dysregulation and metabolic disturbances in promoting accelerated CVD. Understanding how these pathogenic factors promote vascular injury may provide better molecular candidates for therapeutic targeting, and ultimately to improve CVD outcomes.
Wednesday, January 16, 2019
•Retinal vein occlusion is a common cause of vision loss.•Risk factors include hypertension, dyslipidemia, diabetes and obstructive sleep apnea.•Thrombophilia screening is usually not required.•No high-quality evidence exists to support routine use of antithrombotic drugs.•Anticoagulation may be considered in select patients.
Retinal vein occlusion is a common and important cause of vision loss. In general, knowledge about this condition is scant within an internist's practice but the condition is relevant because of its association with other chronic ailments. A diagnosis of RVO should prompt the investigation of conditions needing chronic management in these patients. In this review we summarize the clinical presentation of RVO, its classification, associated risk factors, and treatment focused in the internist's scope of practice.
No, not in my reading of the study. Here’s a summary of the findings:
Objectives: Decreased staffing at nighttime is associated with worse outcomes in hospitalized patients. Rapid response teams were developed to decrease preventable harm by providing additional critical care resources to patients with clinical deterioration. We sought to determine whether rapid response team call frequency suffers from decreased utilization at night and how this is associated with patient outcomes.
Design: Retrospective analysis of a prospectively collected registry database.
Setting: National registry database of inpatient rapid response team calls.
Patients: Index rapid response team calls occurring on the general wards in the American Heart Association Get With The Guidelines-Medical Emergency Team database between 2005 and 2015 were analyzed.
Measurements and Main Results: The primary outcome was inhospital mortality. Patient and event characteristics between the hours with the highest and lowest mortality were compared, and multivariable models adjusting for patient characteristics were fit. A total of 282,710 rapid response team calls from 274 hospitals were included. The lowest frequency of calls occurred in the consecutive 1 AM to 6:59 AM period, with 266 of 274 (97%) hospitals having lower than expected call volumes during those hours. Mortality was highest during the 7 AM hour and lowest during the noon hour (18.8% vs 13.8%; adjusted odds ratio, 1.41 [1.31-1.52]; p less than 0.001). Compared with calls at the noon hour, those during the 7 AM hour had more deranged vital signs, were more likely to have a respiratory trigger, and were more likely to have greater than two simultaneous triggers.
Conclusions: Rapid response team activation is less frequent during the early morning and is followed by a spike in mortality in the 7 AM hour. These findings suggest that failure to rescue deteriorating patients is more common overnight. Strategies aimed at improving rapid response team utilization during these vulnerable hours may improve patient outcomes.
I have no data but my strong subjective impression is that this diurnal pattern existed long before anybody thought up the idea of rapid response teams. Hospital resources are slim at night and are most readily available mid day. 7 AM is shift change in most hospitals. There are a lot of confounders here.
Conclusions and Relevance Among young patients with type 1 diabetes, insulin pump therapy, compared with insulin injection therapy, was associated with lower risks of severe hypoglycemia and diabetic ketoacidosis and with better glycemic control during the most recent year of therapy. These findings provide evidence for improved clinical outcomes associated with insulin pump therapy compared with injection therapy in children, adolescents, and young adults with type 1 diabetes.
Tuesday, January 15, 2019
Objective: 1) Determine frequency and magnitude of delays in second antibiotic administration among patients admitted with sepsis; 2) Identify risk factors for these delays; and 3) Exploratory: determine association between delays and patient-centered outcomes (mortality and mechanical ventilation after second dose).
Design: Retrospective, consecutive sample sepsis cohort over 10 months.
Setting: Single, tertiary, academic medical center.
Patients: All patients admitted from the emergency department with sepsis or septic shock (defined: infection, greater than or equal to 2 systemic inflammatory response syndrome criteria, hypoperfusion/organ dysfunction) identified by a prospective quality initiative. Exclusions: less than 18 years old, not receiving initial antibiotics in the emergency department, death before antibiotic redosing, and patient refusing antibiotics.
Interventions: We determined first-to-second antibiotic time and delay frequency. We considered delay major for first-to-second dose time greater than or equal to 25% of the recommended interval. Factors of interest were demographics, recommended interval length, comorbidities, clinical presentation, location at second dose, initial resuscitative care, and antimicrobial activity mechanism.
Measurements and Main Results: Of 828 sepsis cases, 272 (33%) had delay greater than or equal to 25%. Delay frequency increased dose dependently with shorter recommended interval: 11 (4%) delays for 24-hour intervals (median time, 18.52 hr); 31 (26%) for 12-hour intervals (median, 10.58 hr); 117 (47%) for 8-hour intervals (median, 9.60 hr); and 113 (72%) for 6-hour intervals (median, 9.55 hr). In multivariable regression, interval length significantly predicted major delay (12 hr: odds ratio, 6.98; CI, 2.33–20.89; 8 hr: odds ratio, 23.70; CI, 8.13–69.11; 6 hr: odds ratio, 71.95; CI, 25.13–206.0). Additional independent risk factors were inpatient boarding in the emergency department (odds ratio, 2.67; CI, 1.74–4.09), initial 3-hour sepsis bundle compliance (odds ratio, 1.57; CI, 1.07–2.30), and older age (odds ratio, 1.16 per 10 yr, CI, 1.01–1.34). In the exploratory multivariable analysis, major delay was associated with increased hospital mortality (odds ratio, 1.61; CI, 1.01–2.57) and mechanical ventilation (odds ratio, 2.44; CI, 1.27–4.69).
Conclusions: Major second dose delays were common, especially for patients given shorter half-life pharmacotherapies and who boarded in the emergency department. They were paradoxically more frequent for patients receiving compliant initial care. We observed association between major second dose delay and increased mortality, length of stay, and mechanical ventilation requirement.
Solutions? Better integration of the emergency department with the rest of the hospital might help.
Monday, January 14, 2019
Conclusions—Results from our study of the 3 NOACs versus warfarin in nonvalvular atrial fibrillation patients with a previous history of stroke/transient ischemic attack are relatively consistent with their respective phase III trials and previous stroke/transient ischemic attack subgroup analyses. All NOACs seemed no worse than warfarin in respect to ischemic stroke, ICH, or major bleeding risk.
This is in contrast to what is seen in the real world.
From a paper in Critical Care Medicine:
Although stress cardiomyopathy has been described in association with epilepsy, its frequency in patients with convulsive status epilepticus remains unknown. Accordingly, we sought to determine the prevalence and risk factors of stress cardiomyopathy in patients admitted to the ICU for convulsive status epilepticus.
Prospective, descriptive, single-center study.
Medical-surgical ICU of a teaching hospital.
Thirty-two consecutive ventilated patients (21 men; age, 50 ± 18 yr; Simplified Acute Physiology Score II, 53 ± 15; Sequential Organ Failure Assessment, 6 ± 2) hospitalized in the ICU for convulsive status epilepticus.
MEASUREMENTS AND MAIN RESULTS:
Hemodynamic parameters, transthoracic echocardiography, biological data, and electrocardiogram were obtained serially on ICU admission (H0), and after 6, 12, 24, and 48 hours of hospitalization (H6, H12, H24, and H48). Stress cardiomyopathy was defined as a 20% decrease in left ventricular ejection fraction between H0 or H6 and H48. Stress cardiomyopathy was diagnosed in 18 patients (56%; 95% CI, 38-74%). Mean left ventricular ejection fraction, left ventricular stroke index and cardiac index were initially (at H0 or H6 according to lowest individual values) significantly reduced in stress cardiomyopathy patients (45 ± 14% vs 61 ± 6%, p less than 0.001; 24 ± 8 vs 28 ± 8 mL/m(2), p less than 0.05; 2.3 ± 0.7 vs 3.0 ± 0.8 L/min/m(2), p less than 0.05, respectively) and increased secondarily to reach similar mean values than those observed in patients without transient left ventricular dysfunction at H24. Dobutamine was more frequently used in patients with stress cardiomyopathy. Mean lactate level was increased and significantly higher in stress cardiomyopathy patients at H0 and H6, whereas mean central venous oxygen saturation was preserved but significantly lower in this group. Only three patients with stress cardiomyopathy had left ventricular regional wall motion abnormalities but normal coronary angiography. Risk factors of stress cardiomyopathy were age and Simplified Acute Physiology Score II.
These results suggest that stress cardiomyopathy is common in patients admitted to the ICU for convulsive status epilepticus. Accordingly, these patients should be screened for stress cardiomyopathy and monitored if they present with hemodynamic compromise.