How does fast track affect quality of care in the emergency department?

STUDY OBJECTIVES: Use of fast track has been shown to improve the emergency department flow of less urgent patients. It has been speculated, however, that this could negatively affect the care of urgent patients. The objective of this study was to determine whether a dedicated fast track for less urgent patients [Canadian Triage and Acuity scale category 4/5 (CTAS 4/5)] affected (1) the time to assessment for urgent patients (CTAS 3), (2) the length of stay for less urgent patients (CTAS 4 and 5), and (3) the left-without-being-seen rate. METHODS: In June 2003, fast track was opened in our emergency department from 13:00 to 19:00 h. A before-after intervention comparison analysis was completed for 1 week in Aug 2002 and the same week in Aug 2003. Data collected included (1) time to assessment of CTAS 3 patients, (2) the length of stay for CTAS 4/5 patients, and (3) percentage of patients who left without being seen. RESULTS: A total of 368 patients were reviewed for 2002 and 380 patients were reviewed for 2003. Median time to assessment of CTAS 3 patients presenting from 13:00 to 19:00 h was reduced from 66 min (Interquartile range: 40, 94 min) in 2002 to 60 min (IQR: 38, 108 min) after fast track was open in 2003 (P = 0.95). Median length of stay of CTAS 4 and 5 patients was reduced from 170 min (IQR: 111, 256 min) to 110 min (IQR: 69, 185 min) (P < 0.001). The overall left-without-being-seen rate decreased from 5% (20/368) to 2% (9/380). CONCLUSION: A dedicated fast track for CTAS 4/5 patients can reduce the length of stay and the left-without-being-seen rate with no impact on CTAS 3 patients seen in the main emergency department.     

The ultrastructure of the avian Golgi tendon organ

The ultrastructure of the avian Golgi tendon organ (GTO) is described and compared with those of mammals using transverse sections through the myo-tendinous junctions of wing muscles of adult mallard ducks. The capsule, which is continuous with the perineural epithelial sheath of the Ib afferent nerve fiber, consists of four to seven flattened cellular lamellae. Two to four muscle fibers attach to large collagen bundles which enter the GTO through a tight collar at the proximal end of the fusiform capsule. These collagen bundles divide into many smaller bundles, which run longitudinally through the lumen in compartments formed by septal cells. The septal cells contain many prominent lipid accumulations. The Ib axon divides several times, and the unmyelinated branch axons weave between the small collagen bundles. Schwann cell processes or basement membrane usually intervene between the axons and collagen bundles. The small collagen bundles regroup into larger bundles, which pass through tight capsular collars and merge with the main muscle tendon. The size of the duck GTOs was measured and found to be smaller than the GTOs of man, cat or rat.     

Preclinical evaluation of 2-[4-(7-chloro-2-quinoxalinyloxy)phenoxy]-propionic acid as a modulator of etoposide in human Waldenstrom's macroglobulinemia xenograft model.

We have previously reported that XK469 (2-[4-(7-chloro-2-quinoxalinyloxyphenoxy]-propionic acid) enhances topo IIalpha expression in WSU-WM cells in vitro [E. Mensah-Osman et al., Mol. Cancer Ther., 1: 1321-1326, 2002]. To test the hypothesis that XK469-induced expression of topo IIalpha sensitizes WSU-WM cells to the topo IIalpha inhibitor etoposide (VP-16), we investigated the antitumor effects of XK469 and VP-16 in vivo, using the WSU-WM SCID xenograft model. Individual dosages of XK469 at 20-60 mg/kg/injection i.v. for a maximum-tolerated dose of 240 mg/kg were achievable in SCID mice. Simultaneous administration of a subtherapeutic dose of XK469 (20 mg/kg) and VP-16 at its maximum-tolerated dose of 15 mg/kg proved to be highly toxic and lethal. However, daily sequential treatment of XK469 given i.v. via tail vein at 20 mg/kg for a total of 120 mg/kg, followed 7 h later by VP-16 i.p. at 15 mg/kg for a total of 90 mg/kg, had no significant toxicity in SCID mice. The sequential treatment was associated with enhanced antitumor activity. Tumor growth inhibition T/C, tumor growth delay T-C, and log(10) kill for XK469 alone were 61%, 3 days and 0.46; VP-16 alone 6%, 12 days and 1.83, respectively; whereas the sequential administration of both agents gave a T/C value of 0%, T-C value of 23 days and a log(10) kill of 3.5. On the basis of these animal results, we conclude that the sequential treatment of WSU-WM tumors with XK469 and VP-16 was highly active. The study supports our in vitro observation that XK469 potentiates VP-16 activity. The sequential use of both agents resulted in clinically significant antitumor activity in the WM model.     

Acute pancreatitis in patients on chronic peritoneal dialysis: an increased risk?

OBJECTIVES: The primary aim of this study is to determine if patients with end-stage renal disease (ESRD) on peritoneal dialysis (PD) have a higher risk of developing acute pancreatitis (AP) than patients on hemodialysis (HD). The secondary aim is to compare the outcomes of AP between the two groups. METHOD: This is a retrospective case-control study. The study groups consisted of all patients initiated on HD and PD between January 1, 1998 and August 1, 2003. AP was identified using ICD-9 codes. Statistical analysis was carried out using Poisson regression, Kaplan-Meier curve, log-rank test, and Cox regression. RESULTS: One thousand two hundred and thirty-three and 160 eligible patients were identified in the HD and PD groups, respectively. Twenty-eight patients had AP. Eight patients were excluded as they had identifiable etiologies for AP. Of the remaining 20 patients with AP, 14 were in the HD group and 6 were in the PD group (p= 0.009). Incidence of AP was 18.4 per 1,000 person-years in the PD group and 6.5 per 1,000 person-years in the HD group (p= 0.033). Kaplan-Meier curves showed a significant difference in AP-free survival between the two groups (log-rank p= 0.026). Using time-dependent analysis, the hazard ratio for AP in PD patients after adjustment for age and sex was 3.94 (p= 0.006). There was no observed difference in length of hospital stay and ICU stay. All cases of AP were interstitial. There were no complications or deaths related to AP. CONCLUSION: PD is a risk factor for AP. There is no statistical difference in AP-related mortality and morbidity between HD and PD.     

Efficacy of ombitasvir/paritaprevir/ritonavir/ribavirin in management of HCV genotype 4 and end-stage kidney disease

Background

Till now, pooled data about the safety and efficacy of different direct-acting antiviral (DAAs) regimens in different renal situations are still under evaluation.

Association of total antioxidants level with glaucoma type and severity

Objectives:

To compare the mean total antioxidant status (TAS) among 3 glaucoma types, namely: pseudoexfoliation glaucoma (PEG), primary open angle glaucoma (POAG), and primary angle closure glaucoma (PACG), and study its potential association with various clinical glaucoma-parameters.

Methods:

In this case-control study, plasma samples were obtained between September 2013 and October 2014 from 340 glaucoma patients (PEG [n=54]; POAG [n=147]; PACG [n=139]), and 351 controls of matching age, gender, ethnicity, and 5 different systemic co-morbidities from King Abdulaziz University Hospital, Riyadh, Saudi Arabia. The TAS in all samples was determined by a colorimetric-based assay.

Results:

The mean±standard deviation of TAS was significantly lower among cases: 0.77±0.32 than controls: 1.1±0.22, p<0.0001. Moreover, the TAS levels were significantly different across the 3 types of glaucoma: 0.86±0.24 in PEG, 0.47±0.32 in POAG, and 0.98±0.41 in PACG (all p<0.0001). In addition, there was a significant correlation between TAS and age at onset (Pearson correlation coefficient [R] 0.17, p<0.0001), cup/disc ratio (R: -0.13, p=0.004), and number of anti-glaucoma medications (R: -0.16, p=0.001).

Conclusion:

Our findings provide evidence that plasma TAS levels are decreased in patients with glaucoma, more so in POAG and PEG than PACG, supporting the hypothesis that decreased antioxidative defense and/or increased oxidative stress may have a critical role in the pathogenesis of glaucoma.Glaucoma is a progressive optic neuropathy associated with optic nerve damage, and is one of the most leading cause of blindness worldwide.1 Elevated intraocular pressure (IOP) as a result of reduction in normal aqueous outflow is a major causal risk factor that is well supported by animal studies.2-4 Although IOP is considered a major risk factor for glaucoma,2,3 other concomitant factors affecting the pathophysiology of glaucomatous retinal ganglion cell (RGC) death include retinal ischemia,5 nutritional status,6 and oxidative stress.7 There is evidence of oxidative damage in ocular diseases, such as cataract and age-related macular degeneration.8 In addition, significant oxidative damage has been demonstrated in human trabecular meshwork (TM) cells of patients with glaucoma,7 causing elevated IOP and visual field damage.9 Furthermore, our previous studies have documented mitochondrial abnormalities10-12 (oxidative stress marker), and glutathione-S-transferase (antioxidant) gene (GST) polymorphisms to be associated with various types of glaucoma.13 It is clearly evident from the literature, and our own studies, that oxidative stress mechanisms play a critical role in the pathogenesis of glaucoma. Previous studies had demonstrated reduced total antioxidant capacity in aqueous humor and blood samples from patients with glaucoma.14-17 To evaluate the role of oxidative stress in different types of glaucoma we had previously investigated total antioxidants status (TAS) in the plasma of pseudoexfoliation glaucoma (PEG) patients,18 primary angle closure glaucoma (PACG) patients,19 and in the plasma of primary open angle glaucoma (POAG) patients.20 As an extension to these studies, here, we compare the mean TAS level among these 3 glaucoma types, and study the potential association between the TAS level and various clinical parameters important to each type of glaucoma.18-20