Using a venous thromboembolism checklist significantly improves VTE prevention: a junior doctor led intervention.

AIMS: Given that venous thromboembolic disease is a significant cause of morbidity and mortality, the aim of this study was to increase the rate of VTE risk assessment performed by junior doctors in the acute setting. We also wanted to increase the rates of prescription of thromboembolic preventative measures in those patients whom the assessment identified as being high risk. METHODS: A survey of all patients admitted to three medical wards over a 3-week period was performed to determine whether VTE risk assessment had been performed, and whether prescription of prophylactic measures had been carried out where appropriate. A prompt sheet was subsequently attached to the drug card, and the survey repeated to assess impact on risk assessment and prescription rates. RESULTS: Use of the prompt sheet significantly increased the percentage of patients being appropriately prescribed VTE prophylaxis. CONCLUSIONS/MESSAGE FOR THE CLINIC: Most physicans are aware of the risk of VTE to inpatients, but because of human factors throughout the daily ward activities, VTE assessment can be missed. A simple intervention such as a VTE assessment prompt sheet on the front of the drug card can significantly improve VTE assessment and therefore patient safety.

Serum urea and total cholesterol independently predict re-hospitalisation with a cardiac-related event following an acute ST-elevation myocardial infarction.

BACKGROUND: Although elevated serum urea and low serum sodium have been shown to be associated with increased short-term (30-day) mortality following an ST-elevation myocardial infarction (STEMI), little is known about the role of these biochemical markers as predictors of intermediate-term (1-year) re-hospitalisation. METHODS: Case notes of 90 consecutively admitted patients discharged with a primary diagnosis of an STEMI were retrospectively investigated. Baseline parameters were recorded and patients' clinical course following hospital discharge was carefully reviewed up to 1-year post-STEMI. Multivariate logistic regression analysis was performed to determine the independent association between baseline parameters and 1-year re-hospitalisation. RESULTS: The mean age of the patients was 62.8+/-1.38 years. Thirty patients (33.3%) were re-hospitalised for cardiac-related events and three patients (3.3%) died within 1 year of index STEMI. Using stepwise regression analysis, after adjusting for all independent variables, admission total cholesterol (p=0.013) and urea (p=0.04) were found to be the only significant independent predictors of re-hospitalisation or death. Admission serum sodium was non-significant (p=0.065), but only just. For each mmol/L increase in total cholesterol, a patient was 2.18 times more likely to be re-hospitalised, while for each mmol/L increase in serum urea, a patient was 1.32 times more likely to be re-hospitalised or die. When data were categorised based on high urea (> 7 mmol/L), high total cholesterol (> 5.0 mmol/L) and low sodium (< 135 mmol/L) at admission, none of these variables showed any significant increased risk of re-hospitalisation or death. This suggests that these biochemical parameters were continuously associated with risk of re-hospitalisation through the whole range of serum concentrations. CONCLUSION: In this retrospective study, independent predictors of 1-year re-hospitalisation following an STEMI include high serum urea, raised cholesterol levels and, possibly, reduced sodium levels. These simple biomarkers can be included in patients' risk stratification when following post-STEMI patients in out-patient clinics.

An investigation of leakage tracts along stressed suture lines in phantom tissue.

Suturing is still one of the most important procedures used in trauma and surgery environments. It does however rely on piercing other wise healthy tissue. In doing so channels are opened which may act as conduits for bacteria to enter the body or to allow material such as blood or intestinal bacteria to leak from vessels. This work shows by means of finite element analysis and physical modelling through the use of a phantom that the tension in the suture has a direct bearing on the opening of these channels. It was found that for the phantom the channel cross-sectional area was approximately proportional to the applied tension and suture thread deflection. Leakage channels of up to 0.1mm(2) cross-section were achieved with suture tensions of 120 grammes force. Channels of this size are significantly larger than the bacteria suggesting transmission is theoretically possible.

Attenuated neutrophil respiratory burst following acute hypoglycaemia in diabetic patients and normal subjects.

The effects of insulin-induced hypoglycaemia on the neutrophil respiratory burst were investigated in six patients with type 1 diabetes and six non-diabetic control subjects. Plasma glucose reached similar nadirs in control subjects (0.9 +/- 0.1 mmol 1(-1); mean +/- SEM) and diabetic patients (1.2 +/- 0.2 mmol 1(-1)) (NS). The resting neutrophil respiratory burst was similar in control subjects (1.26 +/- 0.15 mV) and diabetic patients (1.03 +/- 0.18 mV) (NS). The neutrophil respiratory burst fell following hypoglycaemia in control subjects and diabetic patients to 0.38 +/- 0.05 mV (P < 0.001) and 0.54 +/- 0.09 mV (P < 0.05), respectively. This fall was significantly greater in control subjects (ANOVA; P < 0.001). Resting neutrophil counts were not significantly different in control subjects (3.2 +/- 0.3 x 10(9) 1(-1)) and diabetic patients (6.1 +/- 1.5 x 10(9) 1(-1)). Following hypoglycaemia, neutrophil numbers increased in control subjects and diabetic patients to 11.5 +/- 1.4 x 10(9) 1(-1) (P < 0.01) and 9.7 +/- 1.7 x 10(9) 1(-1) (P < 0.05), respectively. This increase was significantly greater in control subjects (ANOVA; P < 0.001). These results suggest that the neutrophil respiratory burst is suppressed in response to hypoglycaemia and that this phenomenon is more pronounced in non-diabetic subjects.

Drinking-driving accident countermeasures: why not try changing the environment?

Effective long-term countermeasures to accidents involving alcohol-impaired drivers are in short supply. Environmental countermeasures, currently the poor relation among drinking-driving countermeasures, may offer some hope in improving this state of affairs. The knowledge needed for the design of appropriate environmental countermeasures is, however, grossly deficient and this needs to be remedied before any real change to the current "countermeasure implementation by guesswork" approach takes place. The paper should be regarded first as a prompt for rethinking current drinking-driving accident countermeasures, and second as a call for more pertinent research on driving behaviour degradation with alcohol intoxication.

The emerging pandemic of obesity and diabetes: are we doing enough to prevent a disaster?

Obesity is growing into a global epidemic and alarming trends are seen in Asian countries. Although obesity is defined by body mass index (BMI), waist circumference has emerged as a more specific marker of metabolic risk. BMI and waist circumference thresholds vary between ethnicities and values are lower for Asian populations. Asians are at an increased risk of developing diabetes and early death from cardiovascular complications at lower levels of BMI and waist circumference. Obesity, especially central obesity is strongly associated with development and worsening of type 2 diabetes. The developing countries may find it difficult to face a surge in diabetes with early death and loss of productivity. Therefore, early action to contain an epidemic of obesity should be considered an urgent global priority.

Diabetes mellitus and stroke.

The aim of this article was to describe (i) the epidemiology and outcomes of stroke relating to diabetes; (ii) the pathophysiology of diabetes as a risk factor for stroke; (iii) the management of acute stroke in patients with diabetes; (iv) the evidence of primary and secondary prevention of stroke in patients with diabetes; and (v) the risk of new-onset diabetes using older antihypertensive agents. The combination of diabetes and stroke disease is a major cause of morbidity and mortality worldwide. Evidence from large clinical trials performed in patients with diabetes supports the need for aggressive and early intervention to target patients' cardiovascular (CV) risks in order to prevent the onset, recurrence and progression of acute stroke. Identification of at-risk patients with diabetes and metabolic syndrome has also allowed the delivery of early and effective intervention to reduce stroke risks, while active treatment during the acute phase of stroke will reduce long-term neurological and functional deficits. While the ongoing debate on the risk benefits of different antihypertensive, lipid-lowering and antiplatelet agents should not detract clinicians from pursuing aggressive CV risk reduction, the application of evidence-based medicine specifically in patients with diabetes will facilitate the use of appropriate agents to improve clinical outcomes. The overall management of patients with diabetes and acute stroke or at risk of secondary stroke should also include multifactorial intervention that not only targets patient's CV risk but also includes behavioural, lifestyle and, where appropriate, surgical intervention.

Diabetes prevention: is there more to it than lifestyle changes?

Over the past years, there has been an explosive increase in the prevalence of type 2 diabetes (T2DM) and this is expected to continue, entailing associated morbidity and mortality. An increasing number of studies explore the different ways T2DM could be prevented. On-going lifestyle modifications need to be addressed. High-risk patients should be given counselling on weight loss, possibly using a low glycaemic index diet, with a target of around 7-10% over 6-12 months, as well as instruction for increasing physical activity to around 150 min of physical exercise weekly (NNT = 4-8). Moderate alcohol consumption and coffee consumption may also be of benefit (NNT = 89 and 66, respectively). Metformin (NNT = 14), acarbose (NNT = 11) and troglitazone (NNT = 6) have been shown to prevent/delay T2DM and angiotensin-converting enzyme (ACE) inhibitors and statins appear to have an adjunctive role (NNT = 42 and 112, respectively). Trials with orlistat and bariatric surgery have also prevented T2DM (NNT = 36 and 6, respectively), and forthcoming treatment with GLP1 mimetics appears promising. Diabetes prevention studies should help create well-defined strategies for screening and treating high-risk populations in the real world, as prevention is our only chance to alleviate the ever growing burden of diabetes mellitus in the world.

Are we good at thromboembolic disease prophylaxis - an audit of the use of risk assessment forms in emergency medical admissions.

Venous thromboembolism (VTE) is a major cause of morbidity and mortality in hospitalised patients. Thromboprophylaxis is an effective strategy for VTE prevention in high-risk patients. An initial audit in our district general hospital trust showed poor adherence to the thromboembolic risk factors consensus group recommendations and so a risk assessment form (RAF) was devised. We present repeated audits to assess the RAF uptake and its effects on VTE thromboprophylaxis. We also present data analysing perceptions among doctors of the RAF and reasons for its poor completion. We provide compelling evidence that the RAF is an invaluable tool in the assessment of VTE thromboprophylaxis.

Hereditary hyperlipidemia in the rabbit due to overproduction of lipoproteins. I. Biochemical studies.

An inherited metabolic disorder in a strain of New Zealand White rabbits, characterized by marked hypercholesterolemia (394 +/- 100 mg/dl), with moderately elevated or normal triglyceride levels is described. Low density lipoprotein (LDL), intermediate density lipoprotein (IDL) and very low density lipoprotein (VLDL) cholesterol levels were increased. VLDL and IDL, and to a lesser extent LDL, had increased free cholesterol and esterified cholesterol content, and triglyceride content was reduced. Kinetic studies with 131I and 125I-labelled rabbit lipoproteins showed a marked increase in production rates of VLDL apo B and LDL apo B. LDL cholesterol levels were directly related to LDL apo B production rate (r = 0.938, p less than 0.001). Both in hypercholesterolemic and normal rabbits injected with labelled VLDL, the specific activity-time curves of VLDL apo B and LDL apo B did not intersect, indicating that LDL apo B was in part derived from sources other than VLDL. No defect was demonstrated in receptor-mediated catabolism of LDL by cultured skin fibroblasts from hyperlipidemic animals. The fractional catabolic rate of LDL apo B was subnormal, but increased when the expanded LDL apo B pool size was reduced by exchange transfusion; the low fractional catabolism may therefore be attributable, at least in part, to saturation of LDL receptors consequent upon the increased pool size of LDL. The hyperlipidemia in this strain of rabbits may be unique in that the underlying mechanism appears to be overproduction of VLDL and LDL.