Friday, August 31, 2018
Thursday, August 30, 2018
Timely post-resuscitation coronary reperfusion therapy is recommended; however, the timing of immediate coronary reperfusion for out-of-hospital cardiac arrest (OHCA) has not been established. We studied the effect of the time interval from arrest to percutaneous coronary intervention (PCI) on resuscitated OHCA patients.
All witnessed OHCA patients with a presumed cardiac etiology received successful PCI at hospitals between 2013 and 2015, excluding cases with unknown information regarding the time from arrest to PCI and survival outcomes. The main exposure of interest was the time interval from arrest to ballooning or stent placement in coronary arteries, and cases were categorized into five groups of 0–90, 90–120, 120–150, and 150–180 min and 3–6 h. The endpoint was survival with good neurological recovery. Multivariable logistic regression analysis was performed, adjusting for patient-community, prehospital, and hospital factors.
A total of 765 patients (24.1% received PCI within 90 min; 31.0% in 90–120 min; 17.8% in 120–150 min; 12.3% in 150–180 min; 14.9% in 3–6 h after arrest) were included. Good neurological recovery was more frequent in the early PCI groups than the delayed PCI group (63.6%, 55.3%, 47.8%, 33.0%, and 42.1%, respectively). The adjusted OR (95% CI) for good neurological recovery compared with the most early PCI group was 0.86 (0.53–1.39) in the PCI group between 90 and 120 min; 0.76 (0.45–1.31) in the PCI group between 120 and 150 min; 0.42 (0.22–0.79) in the PCI group between 150 and 180 min; and 0.53 (0.30–0.93) in PCI group after 3 h.
Among resuscitated OHCA patients with a presumed cardiac etiology and successful PCI, patients who received a delayed coronary intervention after 150 min from arrest were less likely to have neurologically intact survival compared to those who received an early intervention.
For archived events prior to 4/19/18 click here.
8/2/18 Histoplasmosis, blastomycosis. Michael Saccente MD
7/26/18 The Hospitalized Parkinsons patient. Rohit Dhall MD
7/19/18 Cognition, frailty and survivorship: braving the intangibles of critical illness. Emily Kocurek MD
6/24/18 What’s so diff-icult about C diff? Atul Kothari MD
6/21/18 Update in perioperative medicine. Latha Achanta MD
6/14/18 Caring for patients with acute liver failure. Katie Rude MD
6/7/18 iPSC-exosomes for precision medicine for heart failure. Phillip C Yang MD
5/17/18 Alpha-gal red meat allergy: an emerging epidemic of anaphylaxis? Scott P. Commins MD
5/10/18 CAR-T cell therapy toxicity management. Appalla Naidu Sasapu MD
4/26/18 SBE prophylaxis: the myth of sisyphus. What’s the harm? Walter R Wilson MD
4/19/18 Chronic kidney disease mineral and bone disorder (CKD-MBD) originally known as renal osteodystrophy. Robert S Weinstein MD
Saturday, August 11, 2018
From a recent review:
Clinical presentation is heterogeneous with most patients presenting with cranial nerve palsy, headache, or sensory abnormalities. Patients are classified according to probability of the diagnosis with the Zajicek criteria. In these criteria, histopathological confirmation of noncaseating granulomas in affected tissue outside the nervous system is key. Radiological abnormalities on neuroimaging are nonspecific. No biomarkers have been described that adequately identify patients with sarcoidosis. However, soluble interleukin-2 receptor is a relatively novel biomarker that may be useful. In addition to HRCT scan, 18 F-FDG PET-CT scanning can identify occult locations of disease activity and aid in obtaining pathological confirmation. Despite the use of new therapies, still a third of patients remains stable, deteriorate, or die.
Diagnosing and treating patients with neurosarcoidosis remains a challenge. Long-term prospective studies evaluating patients suspected of neurosarcoidosis are needed to assess sensitivity and specificity of ancillary investigations and diagnostic criteria. Furthermore, future studies are needed to evaluate the prognosis and the optimal treatment strategy.
Friday, August 10, 2018
Thursday, August 09, 2018
As pointed out in this free full text review the neuropsychiatric side effects go beyond impulsive gambling to a variety of impulse control phenomena and other psychiatric disturbances. Moreover, it’s not just in patients treated with Parkinson disease but also some of those treated for restless leg syndrome and prolactinoma. There are a number of poorly understood metabolic effects as well, largely favorable it would seem.
Wednesday, August 08, 2018
From a recent paper:
Nonalcoholic fatty liver disease (NAFLD) is independently linked to cardiometabolic morbidity and mortality. Low-grade inflammation, oxidative stress and ectopic fat, common features of chronic obstructive pulmonary disease (COPD), might contribute to the development of NAFLD.
We aimed to investigate the prevalence of NAFLD and to evaluate the relationship between various types of liver damage and COPD severity, comorbidities and circulating inflammatory cytokines. Validated noninvasive tests (FibroMax: SteatoTest, NashTest and FibroTest) were used to assess steatosis, nonalcoholic steatohepatitis (NASH) and liver fibrosis. Patients underwent an objective assessment of COPD comorbidities, including sleep studies. Biological parameters included a complete lipid profile and inflammatory markers.
In COPD patients the prevalence of steatosis, NASH and fibrosis were 41.4%, 36.9% and 61.3%, respectively. In multivariate analysis, SteatoTest and FibroTest were significantly associated with sex, body mass index (BMI), untreated sleep apnoea and insulin resistance, and, in addition, COPD Global Initiative for Chronic Obstructive Lung Disease stage for SteatoTest. Patients with steatosis had higher tumour necrosis factor-α levels and those with NASH or a combination of liver damage types had raised leptin levels after adjustment for age, sex and BMI.
We concluded that NAFLD is highly prevalent in COPD and might contribute to cardiometabolic comorbidities.
Tuesday, August 07, 2018
From a recent review:
Both genetic and epidemiological evidence point towards an autoimmune mechanism in the destruction of orexin/hypocretin neurons. Recent studies suggest both humoral and cellular immune responses in the disease development.
Narcolepsy is a severe sleep disorder, in which neurons producing orexin/hypocretin in the hypothalamus are destroyed. The core symptoms of narcolepsy are debilitating, extreme sleepiness, cataplexy, and abnormalities in the structure of sleep. Both genetic and epidemiological evidence point towards an autoimmune mechanism in the destruction of orexin/hypocretin neurons. Importantly, the highest environmental risk is seen with influenza-A infection and immunization. However, how the cells are destroyed is currently unknown. In this review we summarize the disease symptoms, and focus on the immunological findings in narcolepsy. We also discuss the environmental and genetic risk factors as well as propose a model for disease development.
Monday, August 06, 2018
Sunday, August 05, 2018
Saturday, August 04, 2018
Friday, August 03, 2018
The objective was to determine the relationship between short-term mortality and intravenous morphine use in ED patients who received a diagnosis of acute heart failure (AHF).
Consecutive patients with AHF presenting to 34 Spanish EDs from 2011 to 2014 were eligible for inclusion. The subjects were divided into those with (M) or without IV morphine treatment (WOM) groups during ED stay. The primary outcome was 30-day all-cause mortality, and secondary outcomes were mortality at different intermediate time points, in-hospital mortality, and length of hospital stay. We generated a propensity score to match the M and WOM groups that were 1:1 according to 46 different epidemiological, baseline, clinical, and therapeutic factors. We investigated independent risk factors for 30-day mortality in patients receiving morphine.
We included 6,516 patients (mean age, 81 [SD, 10] years; 56% women): 416 (6.4%) in the M and 6,100 (93.6%) in the WOM group. Overall, 635 (9.7%; M, 26.7%; WOM, 8.6%) died by day 30. After propensity score matching, 275 paired patients constituted each group. Patients receiving morphine had a higher 30-day mortality (55 [20.0%] vs 35 [12.7%] deaths; hazard ratio, 1.66; 95% CI, 1.09-2.54; P = .017). In patients receiving morphine, death was directly related to glycemia (P = .013) and inversely related to the baseline Barthel index and systolic BP (P = .021) at ED arrival (P = .021). Mortality was increased at every intermediate time point, although the greatest risk was at the shortest time (at 3 days: 22 [8.0%] vs 7 [2.5%] deaths; OR, 3.33; 95% CI, 1.40-7.93; P = .014). In-hospital mortality did not increase (39 [14.2%] vs 26 [9.1%] deaths; OR, 1.65; 95% CI, 0.97-2.82; P = .083) and LOS did not differ between groups (median [interquartile range] in M, 8 ; WOM, 8 ; P = .79).
This propensity score-matched analysis suggests that the use of IV morphine in AHF could be associated with increased 30-day mortality.