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Background Endoscopy within 24 h of admission (early endoscopy) is a quality standard in acute upper gastrointestinal bleeding (AUGIB). We aimed to audit time to endoscopy outcomes and identify factors affecting delayed endoscopy (>24 h of admission).Methods This prospective multicentre audit enrolled patients admitted with AUGIB who underwent inpatient endoscopy between November and December 2017. Analyses were performed to identify factors associated with delayed endoscopy, and to compare patient outcomes, including length of stay and mortality rates, between early and delayed endoscopy groups.Results Across 348 patients from 20 centres, the median time to endoscopy was 21.2 h (IQR 12.0–35.7), comprising median admission to referral and referral to endoscopy times of 8.1 h (IQR 3.7–18.1) and 6.7 h (IQR 3.0–23.1), respectively. Early endoscopy was achieved in 58.9%, although this varied by centre (range: 31.0–87.5%, p = 0.002). On multivariable analysis, lower Glasgow–Blatchford score, delayed referral, admissions between 7:00 and 19:00 hours or via the emergency department were independent predictors of delayed endoscopy. Early endoscopy was associated with reduced length of stay (median difference 1 d; p = 0.004), but not 30-d mortality (p = 0.344).Conclusions The majority of centres did not meet national standards for time to endoscopy. Strategic initiatives involving acute care services may be necessary to improve this outcome.

Endoscopy within 24?h of admission (early endoscopy) is a quality standard in acute upper gastrointestinal bleeding (AUGIB). We aimed to audit time to endoscopy outcomes and identify factors affecting delayed endoscopy (>24?h of admission). This prospective multicentre audit enrolled patients admitted with AUGIB who underwent inpatient endoscopy between November and December 2017. Analyses were performed to identify factors associated with delayed endoscopy, and to compare patient outcomes, including length of stay and mortality rates, between early and delayed endoscopy groups. Across 348 patients from 20 centres, the median time to endoscopy was 21.2?h (IQR 12.0–35.7), comprising median admission to referral and referral to endoscopy times of 8.1?h (IQR 3.7–18.1) and 6.7?h (IQR 3.0–23.1), respectively. Early endoscopy was achieved in 58.9%, although this varied by centre (range: 31.0–87.5%, p?=?0.002). On multivariable analysis, lower Glasgow–Blatchford score, delayed referral, admissions between 7:00 and 19:00 hours or via the emergency department were independent predictors of delayed endoscopy. Early endoscopy was associated with reduced length of stay (median difference 1 d; p?=?0.004), but not 30-d mortality (p?=?0.344). The majority of centres did not meet national standards for time to endoscopy. Strategic initiatives involving acute care services may be necessary to improve this outcome.

BackgroundPercutaneous endoscopic gastrostomy (PEG) tubes allow for long-term enteral feeding. Disk-retained PEG tubes may be suitable for long-term usage without planned replacement, but data on longevity are limited. We aimed to assess the rates and predictors of PEG longevity and post-PEG mortality.DesignSingle-centred retrospective cohort study of patients with disk-retained (Freka) PEG tubes.MethodsAll patients undergoing PEG between 2010 and 2013 were identified, and retrospective analysis of outcomes until 2017 (median 1062 days) was performed. Time-to-event data were plotted using Kaplan-Meier curves, with predictors of survival derived from multivariate Cox-regression analyses.Results277patients were studied, with a median age of 74 years (IQR 59–82). PEG tube failure occurred in 17.4%, due to: buried bumper syndrome (7.0%), split/broken tube (6.3%), peristomal infection (1.8%) and dislodged tube (1.1%). PEG tube longevity was 95.1% (1 year) and 68.5% (5 year), with age <70 (HR 2.65, 95% CI 1.25 to 5.62, p=0.011) being predictive of PEG failure. Post-PEG mortality was 10.5% (30 day), 35.4% (1 year) and 59.7% (5 year). Age ≥70 was associated with mortality (HR 2.79, 95% CI 1.92 to 4.05, p<0.001), whereas PEG failure (HR 0.46, 95% CI 0.27 to 0.77, p=0.003) and elective PEG removal (HR 0.23, 95% CI 0.08 to 0.64, p=0.005) were associated with reduced mortality.Conclusions68.5% of PEG tubes remain intact after 5 years. Younger age was associated with earlier PEG failure, whereas younger age, PEG replacement and elective PEG tube removal were associated with improved survival. These data may inform future guidance for elective PEG tube replacements.

Liver transplant recipients are at risk of chronic renal disease, principally as a result of nephrotoxicity of the commonly used immunosuppressive agents cyclosporine and tacrolimus. We have investigated the incidence of chronic renal failure and its risk factors in our transplant population, which was treated predominantly with cyclosporine.

Alcoholic liver disease is associated with three histologically distinct processes: steatosis (parenchymal fat accumulation), alcoholic hapatitis (characterized by parenchymal infiltration by neutrophil polymorphs), and alcoholic cirrhosis (in which chronic inflammation and fibrosis dominate). Chemokines are cytokines that promote subset‐specific leukoycte recruitment to tissues and could therefore play a crucial role in determining which leukocyte subsets are recruited to the liver in alcoholic liver disease. This paper reports that chemokine expression is increased in the liver of patients with alcoholic liver disease and, moreover, that distinct patterns of chemokine expression are associated with the different inflammatory responses to alcohol. Interleukin‐8 (IL‐8), monocyte chemoattractant protein‐1 (MCP‐1), macrophage inflammatory protein‐1α (MIP‐1α), and MIP‐1β were all detected in the parenchyma at sites of inflammation in alcoholic hepatitis, whereas in alcoholic cirrhosis, chemokines were restricted to inflammatory cells and endothelium in the fibrous septa and portal tracts. In alcoholic hepatitis, chemokine transcription was localized to sinusoidal cells, leukocytes, and fibroblasts in areas of parenchymal inflammation, but hepatocytes, despite staining strongly for chemokine protein, were negative. In alcoholic cirrhosis, chemokine mRNA was detected in portal tract endothelium, leukocytes, and fibroblasts. Thus, alcoholic hepatitis and alcoholic cirrhosis are associated with distinct patterns of chemokine expression that are likely to be important factors in determining whether a patient develops acute parenchymal inflammation and alcoholic hepatitis, or chronic septal inflammation and alcoholic cirrhosis. © 1998 John Wiley & Sons, Ltd.

Alcoholic liver disease is associated with three histologically distinct processes: steatosis (parenchymal fat accumulation), alcoholic hapatitis (characterized by parenchymal infiltration by neutrophil polymorphs), and alcoholic cirrhosis (in which chronic inflammation and fibrosis dominate). Chemokines are cytokines that promote subset-specific leukoycte recruitment to tissues and could therefore play a crucial role in determining which leukocyte subsets are recruited to the liver in alcoholic liver disease. This paper reports that chemokine expression is increased in the liver of patients with alcoholic liver disease and, moreover, that distinct patterns of chemokine expression are associated with the different inflammatory responses to alcohol. Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), and MIP-1β were all detected in the parenchyma at sites of inflammation in alcoholic hepatitis, whereas in alcoholic cirrhosis, chemokines were restricted to inflammatory cells and endothelium in the fibrous septa and portal tracts. In alcoholic hepatitis, chemokine transcription was localized to sinusoidal cells, leukocytes, and fibroblasts in areas of parenchymal inflammation, but hepatocytes, despite staining strongly for chemokine protein, were negative. In alcoholic cirrhosis, chemokine mRNA was detected in portal tract endothelium, leukocytes, and fibroblasts. Thus, alcoholic hepatitis and alcoholic cirrhosis are associated with distinct patterns of chemokine expression that are likely to be important factors in determining whether a patient develops acute parenchymal inflammation and alcoholic hepatitis, or chronic septal inflammation and alcoholic cirrhosis. © 1998 John Wiley & Sons, Ltd.