A pragmatic digital health informatics based approach for aiding clinical prioritisation and reducing backlog of care: A study in cohort of 4022 people with diabetes.

BACKGROUND AND AIMS: The backlog of care in resource stretched healthcare systems requires innovative approaches to aid clinical prioritisation. Our aim was to develop an informatics tool to identify and prioritise people with diabetes who are likely to deteriorate whilst awaiting an appointment to optimise clinical outcomes and resources. MATERIALS AND METHODS: Using data from electronic health care records we identified 6 risk-factors that could be addressed in 4022 people (52% male, 30% non-Caucasian) with diabetes attending a large university hospital in London. The risk-factors were new clinical events/data occurring since their last routine clinic visit. To validate and compare data-led prioritisation tool to a traditional 'clinical approach' a sample of 450 patients were evaluated. RESULTS: Of the 4022 people, 549 (13.6%) were identified as having one or more risk events/factors. People with risk were more likely to be non-Caucasian and had greater socio-economic deprivation. Taking clinical prioritisation as the gold standard, informatics tool identified high risk patients with a sensitivity of 83% and lower risk patients with a specificity of 81%. An operational pilot pathway over 3 months using this approach demonstrated in 101 high risk people that 40% received interventions/care optimisation to prevent deterioration in health. CONCLUSION: A pragmatic data-driven method identifies people with diabetes at highest need for clinical prioritisation within restricted resources. Health informatics systems such as our can enhance care and improve operational efficiency and better healthcare delivery for people with diabetes.

Using Trust databases to identify predictors of late booking for antenatal care within the UK.

OBJECTIVES: To identify predictors of late booking for antenatal care using routinely collected data. STUDY DESIGN: Retrospective cohort study. METHODS: Variables were selected with reference to comprehensive literature review. Data were extracted from a London hospital case-note database, and predictors of late booking were identified using logistic regression. RESULTS: In total, 5629 women were included in the study. Median gestation at booking was 14 weeks, and 31% of women booked after 18 weeks of gestation. Variables with insufficient data recorded included language abilities, nationality and social risk. Women aged between 15 and 19 years, women with more than four children, and women belonging to the ethnic group 'other' were all significantly more likely to book late. Women with a body mass index ≥30kg/m(2) were 1.5 times more likely to book late (not significant). CONCLUSION: Case-note databases are a potentially easy and effective way to analyse access to care and provider compliance with quality standards. Current deficits in routine data collection need to be addressed urgently in order to make this possible.

Internal jugular vein thrombosis after assisted conception therapy.

Superovulation therapy during assisted conception may result in a hypercoagulable state. Five cases of upper extremity venous thrombosis were identified in women who conceived after ovarian stimulation for in vitro fertilization (IVF). They presented between 7 and 10 weeks' gestation with neck pain and swelling. Three had been treated for ovarian hyperstimulation syndrome and two had evidence of inherited thrombophilia. Four patients received thromboprophylaxis before presentation. Although thrombosis is an uncommon complication of IVF, patients should be counselled before treatment. Thrombophilia screening may be considered for 'high-risk' patients, although current regimes for thromboprophylaxis remain suboptimal.

The production of interleukin-1beta from human fetal membranes is not obligatory for increased prostaglandin output.

Bacterial endotoxin increased the expression of mRNA (maximal after 4 hr) for interleukin-1beta (IL-1beta) and the release of mature protein from intact human fetal membranes. In contrast, the change in expression of mRNA for type 2 cyclo-oxygenase (COX-2) was biphasic, with peaks after 0.5-1 hr and after 8 hr of culture. An antibody to IL-1beta was without effect after 4 hr of culture, inhibited endotoxin-stimulated prostaglandin E2 (PGE2) production after 8 hr of culture, and caused a parallel decrease in the expression of mRNA for COX-2. We conclude that endotoxin induced the expression of COX-2 through IL-1beta-independent and IL-1beta-dependent mechanisms, and these differences are time dependent. Corticotrophin-releasing hormone (CRH) or platelet-activating factor (PAF) also increased the expression of mRNA for IL-1beta and the release of IL-1beta from some, but not all, fetal membranes. The antibody to IL-1beta did not affect CRH-stimulated or PAF-stimulated PGE2 production or COX-2 expression. We conclude that CRH and PAF can induce the expression of IL-1beta, but this is not obligatory for increased PGE2 release, and the effect of these stimuli on COX-2 expression is a direct, IL-1beta-independent effect.

Stimulation of prostaglandin production from intact human fetal membranes by bacteria and bacterial products.

The addition of live or sonicated Escherichia coli, or endotoxin from E. coli increased the release of prostaglandins (PG) on both sides of intact human fetal membranes after 24 h of incubation, indicating that live bacteria were not required to activate prostaglandin production. Time-course studies showed that the levels of PGE2 and PGF2alpha on the fetal side of the membrane were increased 6 h after the addition of endotoxin, whereas levels on the maternal side increased within 1-2 h. These changes were independent of the side to which the endotoxin was added, indicating that a stimulatory factor passes through the fetal membranes. This factor is not endotoxin, which did not cross the membranes, and further studies are required to identify this endogenous stimulus. Prostaglandin metabolite levels were either unaffected or increased by endotoxin, indicating that the main effect is at the level of increased prostaglandin biosynthesis rather than decreased metabolism.