Effect of a contact monitoring system with immediate visual feedback on hand hygiene compliance.

BACKGROUND: Hand hygiene compliance is traditionally monitored by visual methods that are open to bias and strictly limited in time and place. Automatic monitoring may be more effective for infection control as well as performance management. AIM: To establish accuracy and acceptability of an automatic contact monitoring system for hand hygiene. METHODS: Monitoring equipment was installed across 55 beds in three wards, and included modified identity badges, bedside furniture, sinks and alcohol gel dispensers. Badges were in near-skin contact (through uniform) and could detect alcohol vapour. All devices were linked by wi-fi. A traffic light system on the badge provided immediate feedback to staff and patients on the hand hygiene status of a member of staff on approach to a patient. Compliance was logged automatically. Following a period of immediate feedback, no visual feedback was given for two weeks. Subsequently, feedback was given using red/green lights for 10 days, followed by retrospective feedback to the ward. Hand hygiene was verified independently by an observer. FINDINGS: Hand hygiene compliance increased from 21% of 97 opportunities to 66% of 197 opportunities during active immediate feedback. Compliance decreased when feedback was provided to wards retrospectively. Six staff (26%) avoided wearing a badge, saying that it was too heavy or they were not on the ward all day. Only three of 30 patients stated that they would challenge staff who had not performed hand hygiene. CONCLUSIONS: Automatic contact monitoring with immediate feedback was effective in increasing hand hygiene compliance, but feedback given retrospectively did not prevent a decrease in compliance.

Ascertainment of occupational histories in the working population: the occupational history calendar approach.

BACKGROUND: self-reported occupational histories are an important means for collecting historical data in epidemiological studies. An occupational history calendar (OHC) has been developed for use alongside a national occupational hazard surveillance tool. This study presents the systematic development of the OHC and compares work histories collected via this calendar to those collected via a traditional questionnaire. METHODS: the paper describes the systematic development of an OHC for use in the general working population. A comparison of data quality and recall was undertaken in 51 participants where both tools were administered. RESULTS: the OHC enhanced job recall compared with the traditional questionnaire. Good agreement in the data captured by both tools was observed, with the exception of hazard exposures. CONCLUSIONS: a calendar approach is suitable for collecting occupational histories from the general working population. Despite enhancing job recall the OHC approach has some shortcomings outweighing this advantage in large-scale population surveillance.

Ward assessment of SmartIdeas Project: bringing source isolation to the patient.

Most UK hospitals lack enough single rooms to provide source isolation for all infected patients. The aim of this study was to test prototype isolation systems on general wards together with specifically designed portable sink units and toilets. Questionnaires were offered to staff, patients and visitors covering ease of use and acceptability. A total of 53 patients were isolated, with concurrent collection of environmental samples and staff hand hygiene audit. Blocking of beds next to infected patients was avoided but patients and staff were concerned about limited space and communication. Hand hygiene compliance on entry or exit to/from an isolated bed space significantly improved [43/76 (56.6%) to 107/147 (72.8%), P<0.05]. Although popular, the toilets were mechanically unreliable. Low levels of microbial contamination (<1-3.4cfu/cm(2)) were present within all isolated bed spaces. The highest colony counts were obtained from high contact sites (e.g. remote controls). Meticillin-resistant Staphylococcus aureus (MRSA) was present at similar levels inside all systems. Although one system was designed to provide airborne as well as contact isolation, MRSA was isolated from air inside and outside the system suggesting poor efficiency of the air door. The finding was confirmed by aerobiology tests at the Health Protection Agency Laboratory, Porton Down, UK. A trial of redesigned units is required to establish efficacy (Trial Identifier: ISRCTN02681602).

Hypoglycaemia: the limiting factor in the glycaemic management of Type I and Type II diabetes.

Hypoglycaemia is the limiting factor in the glycaemic management of diabetes. Iatrogenic hypoglycaemia is typically the result of the interplay of insulin excess and compromised glucose counterregulation in Type I (insulin-dependent) diabetes mellitus. Insulin concentrations do not decrease and glucagon and epinephrine concentrations do not increase normally as glucose concentrations decrease. The concept of hypoglycaemia-associated autonomic failure (HAAF) in Type I diabetes posits that recent antecedent iatrogenic hypoglycaemia causes both defective glucose counterregulation (by reducing the epinephrine response in the setting of an absent glucagon response) and hypoglycaemia unawareness (by reducing the autonomic and the resulting neurogenic symptom responses). Perhaps the most compelling support for HAAF is the finding that as little as 2 to 3 weeks of scrupulous avoidance of hypoglycaemia reverses hypoglycaemia unawareness and improves the reduced epinephrine component of defective glucose counterregulation in most affected patients. The mediator and mechanism of HAAF are not known but are under active investigation. The glucagon response to hypoglycaemia is also reduced in patients approaching the insulin deficient end of the spectrum of Type II (non-insulin-dependent) diabetes mellitus, and glycaemic thresholds for autonomic (including epinephrine) and symptomatic responses to hypoglycaemia are shifted to lower plasma glucose concentrations after hypoglycaemia in Type II diabetes. Thus, patients with advanced Type II diabetes are also at risk for HAAF. While it is possible to minimise the risk of hypoglycaemia by reducing risks -- including a 2 to 3 week period of scrupulous avoidance of hypoglycaemia in patients with hypoglycaemia unawareness -- methods that provide glucose-regulated insulin replacement or secretion are needed to eliminate hypoglycaemia and maintain euglycaemia over a lifetime of diabetes.

Hypoglycemia-associated autonomic failure in diabetes.

Hypoglycemia is the limiting factor in the glycemic management of diabetes. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent antecedent iatrogenic hypoglycemia causes both defective glucose counterregulation (by reducing the epinephrine response to falling glucose levels in the setting of an absent glucagon response) and hypoglycemia unawareness (by reducing the autonomic and the resulting neurogenic symptom responses) and thus a vicious cycle of recurrent hypoglycemia. Perhaps the most compelling support for HAAF is the finding that as little as 2-3 wk of scrupulous avoidance of hypoglycemia reverses hypoglycemia unawareness and improves the reduced epinephrine component of defective glucose counterregulation in most affected individuals. Insight into this pathophysiology has led to a broader view of the clinical risk factors for hypoglycemia to include indexes of compromised glucose counterregulation and provided a framework for the study of the mechanisms of iatrogenic hypoglycemia and, ultimately, its elimination from the lives of people with diabetes.

Popped eye (blunt trauma leading to penetrating eye injury and lens displacement in the pseudophakic eye).

Blunt trauma to the eye of patients with an artificial intraocular lens may cause globe rupture with all the accompanying sequelae. It must be recognised promptly and dealt with appropriately before urgent referral to ophthalmology.

Investigation of bias after data linkage of hospital admissions data to police road traffic crash reports.

RESEARCH QUESTION: Does a database of hospital admission data linked to police road traffic accident (RTA) reports produce less biased information for the injury prevention policymaker, planner, and practitioner than police RTA reports alone? DESIGN: Data linkage study. STUDY POPULATION: Non-fatal injury victims of road traffic crashes in southern England who were admitted to hospital. DATA SOURCES: Hospital admissions and police RTA reports. MAIN OUTCOME MEASURES: The estimated proportion of road traffic crashes admitted to hospital that were included on the linked database; distributions by age, sex, and road user groups: (A) for all RTA injury admissions and (B) for RTA serious injury admissions defined by length of stay or by nature of injury. RESULTS: An estimated 50% of RTA injury admissions were included on the linked database. When assessing bias, admissions data were regarded as the "gold standard". The distributions of casualties by age, sex, and type of road user showed major differences between the admissions data and the police RTA injury data of comparable severity. The linked data showed smaller differences when compared with admissions data. For RTA serious injury admissions, the distributions by age and sex were approximately the same for the linked data compared with admissions data, and there were small but statistically significant differences between the distributions across road user group for the linked data compared with hospital admissions. CONCLUSION: These results suggest that investigators could be misinformed if they base their analysis solely on police RTA data, and that information derived from the linked database is less biased than that from police RTA data alone. A national linked dataset of road traffic crash data should be produced from hospital admissions and police RTA data for use by policymakers, planners and practitioners.

Clusters within a general adult population of alcohol abstainers.

BACKGROUND: Our previous study found that alcohol abstainers use acute services more and preventative services less than safe level drinkers. The observed relationships between four categories of alcohol consumption and service use were J-shaped for acute services and inverted J-shaped for preventive services. The aim of this paper was to further investigate these relationships. METHODS: The design was a health and lifestyle survey of 41 000 randomly-sampled adults in SE England. The response rate was 60%. Distinctive subgroups within the alcohol abstainer group were investigated using cluster analysis, based on socio-demographic and health status variables. Odds ratios for services use for the abstainer clusters, and three alcohol consumption groups were estimated from a logistic regression model which included age, social class, ethnic group, employment status, household composition, whether the respondent was a carer, smoking habit, use of private health insurance, and health status. RESULTS: Two clusters were formed for both males and females. Cluster 1 comprised, on average, older, frailer, and more disabled people. Cluster 2 comprised younger, healthier people, a greater proportion of whom belonged to ethnic minority groups. Cluster 2 had similar rates of use of Accident & Emergency, GP, optician, and dental services compared with safe level drinkers. Cluster 1's rates differed from those of both Cluster 2 and safe level drinkers in almost all instances. CONCLUSIONS: The J- and inverted J-shaped relationships between alcohol consumption and service use are partly explained by a subgroup of abstainers who are older, of less good health, and who use hospital, clinic, and domiciliary healthcare services much more than safe level drinkers.

Blood-to-brain glucose transport, cerebral glucose metabolism, and cerebral blood flow are not increased after hypoglycemia.

Recent antecedent hypoglycemia has been found to shift glycemic thresholds for autonomic (including adrenomedullary epinephrine), symptomatic, and other responses to subsequent hypoglycemia to lower plasma glucose concentrations. This change in threshold is the basis of the clinical syndromes of hypoglycemia unawareness and, in part, defective glucose counterregulation and the unifying concept of hypoglycemia-associated autonomic failure in type 1 diabetes. We tested in healthy young adults the hypothesis that recent antecedent hypoglycemia increases blood-to-brain glucose transport, a plausible mechanism of this phenomenon. Eight subjects were studied after euglycemia, and nine were studied after approximately 24 h of interprandial hypoglycemia ( approximately 55 mg/dl, approximately 3.0 mmol/l). The latter were shown to have reduced plasma epinephrine (P = 0.009), neurogenic symptoms (P = 0.009), and other responses to subsequent hypoglycemia. Global bihemispheric blood-to-brain glucose transport and cerebral glucose metabolism were calculated from rate constants derived from blood and brain time-activity curves-the latter determined by positron emission tomography (PET)-after intravenous injection of [1-(11)C]glucose at clamped plasma glucose concentrations of 65 mg/dl (3.6 mmol/l). For these calculations, a model was used that includes a fourth rate constant to account for egress of [(11)C] metabolites. Cerebral blood flow was measured with intravenous [(15)O]water using PET. After euglycemia and after hypoglycemia, rates of blood-to-brain glucose transport (24.6 +/- 2.3 and 22.4 +/- 2.4 micromol. 100 g(-1). min(-1), respectively), cerebral glucose metabolism (16.8 +/- 0.9 and 15.9 +/- 0.9 micromol. 100 g(-1). min(-1), respectively) and cerebral blood flow (56.8 +/- 3.9 and 53.3 +/- 4.4 ml. 100 g(-1). min(-1), respectively) were virtually identical. These data do not support the hypothesis that recent antecedent hypoglycemia increases blood-to-brain glucose transport during subsequent hypoglycemia. They do not exclude regional increments in blood-to-brain glucose transport. Alternatively, the fundamental alteration might lie beyond the blood-brain barrier.

Hypoglycemia risk reduction in type 1 diabetes.

Hypoglycemia is the limiting factor in the glycemic management of diabetes because it generally precludes maintenance of euglycemia. Improving glycemic control while minimizing hypoglycemia in type 1 diabetes mellitus (T1 DM) involves both application of the principles of aggressive therapy--patient education and empowerment, frequent self monitoring of blood glucose, flexible insulin regimens, individualized glycemic goals and ongoing professional guidance and support--and implementation of hypoglycemia risk reduction. Iatrogenic hypoglycemia is the result of the interplay of therapeutic insulin excess and compromised physiological and behavioral defenses against falling plasma glucose concentrations in T1 DM. Relative or absolute insulin excess occurs when insulin doses are excessive, ill-timed or of the wrong type, when exogenous glucose delivery, endogenous glucose production or insulin clearance are decreased or when insulin-independent glucose utilization or sensitivity to insulin are increased. But these conventional risk factors explain only a minority of episodes of severe hypoglycemia. More potent risk factors include absolute insulin deficiency, a history of severe hypoglycemia and aggressive therapy per se as evidenced by lower glycemic goals, lower hemoglobin A1c levels, or both. These are clinical surrogates of compromised glucose counterregulation, the clinical syndromes of defective glucose counterregulation (the result of absent decrements in insulin and absent increments in glucagon with attenuated increments in epinephrine) and hypoglycemia unawareness (the result of reduced autonomic [sympathochromaffin] activation causing reduced warning symptoms of developing hypoglycemia). The unifying concept of hypoglycemia-associated autonomic failure in T1 DM posits that: (1) Periods of relative or absolute therapeutic insulin excess in the setting of absent glucagon responses lead to episodes of hypoglycemia. (2) These episodes, in turn, cause reduced autonomic (including adrenomedullary) responses to falling glucose concentrations on subsequent occasions. (3) These reduced autonomic responses result in both reduced symptoms of developing hypoglycemia (i.e., hypoglycemia unawareness) and--because epinephrine responses are reduced in the setting of absent glucagon responses--impaired physiological defenses against developing hypoglycemia (i.e., defective glucose counterregulation). Thus a vicious cycle of recurrent hypoglycemia is created and perpetuated. Hypoglycemia risk reduction includes, first, addressing the issue of hypoglycemia--the patient's awareness of and concerns about it, its frequency, severity, timing and clinical settings--in every patient contact. Then it requires application of the principles of aggressive therapy, consideration of both the conventional risk factors and those indicative of compromised glucose counterregulation and appropriate regimen adjustments including a two to three week period of scrupulous avoidance of hypoglycemia in patients with hypoglycemia-associated autonomic failure. With this approach the goals of improving glycemic control and minimizing hypoglycemia are not incompatible.

Why the government was right to change the 'Our Healthier Nation' accidental injury target.

We congratulate the current UK Government on their inclusion of accidental injury as one of the national targets in the White Paper: Saving Lives-Our Healthier Nation (OHN). We had concerns about the particular target that was proposed in the Green Paper: 'ellipsisto reduce the rate of accidents-here being defined as those which involve a hospital visit or consultation with a family doctor-by at least a fifthellipsis'. The limitations of this target were: firstly, it would focus attention on minor injury and so not reflect the main burden of injury; and secondly, that ascertainment of cases would be influenced by social factors as well as provision of service and access factors. The new target stated in Saving Lives also has its limitations since it will be influenced by service factors. This target is to reduce by 10% the rate of serious injury, defined as injury resulting in four or more days in hospital. We have proposed the use of an alternative indicator of unintentional injury occurrence, based on serious long bone fracture admitted to the hospital. This alternative indicator is based on the occurrence of serious rather than minor injury. It is likely that a high proportion of cases of these injuries can be identified from existing data sources. Ascertainment of cases is likely to be independent of social, service or access factors. Finally, these injuries are associated with significant long term outcomes including disablement, reduced functional capacity and reduced quality of life. It does have the limitation that it does not measure all serious injury. Such a measure is much more difficult to achieve. Further improvements to our proposed indicator could be made in a number of ways, through investigating an extended definition of the indicator to include a range of other serious injuries, improving the quality of existing data, making other data sources available, including outpatient data, and making serious injury a notifiable disease.

Symptoms of hypoglycemia, thresholds for their occurrence, and hypoglycemia unawareness.

Ultimately traceable to neural glucose deprivation, symptoms of hypoglycemia include neurogenic (autonomic) and neuroglycopenic symptoms. Neurogenic symptoms (tremulousness, palpitations, anxiety, sweating, hunger, paresthesias) are the results of the perception of physiologic changes caused by the autonomic nervous system's response to hypoglycemia. Neuroglycopenic symptoms (confusion, sensation of warmth, weakness or fatigue, severe cognitive failure, seizure, coma) are the results of brain glucose deprivation itself. Glycemic thresholds for symptoms of hypoglycemia shift to lower plasma glucose concentrations following recent episodes of hypoglycemia, leading to the syndrome of hypoglycemia unawareness--loss of the warning symptoms of developing hypoglycemia. Thus, patients with recurrent hypoglycemia (e.g., those with tightly controlled diabetes or with an insulinoma) often tolerate abnormally low plasma glucose concentrations without symptoms.

Insulin resistance in HIV protease inhibitor-associated diabetes.

BACKGROUND: Fasting hyperglycemia has been associated with HIV protease inhibitor (PI) therapy. OBJECTIVE: To determine whether absolute insulin deficiency or insulin resistance with relative insulin deficiency and an elevated body mass index (BMI) contribute to HIV PI-associated diabetes. DESIGN: Cross-sectional evaluation. PATIENTS: 8 healthy seronegative men, 10 nondiabetic HIV-positive patients naive to PI, 15 nondiabetic HIV-positive patients receiving PI (BMI = 26 kg/m2), 6 nondiabetic HIV-positive patients receiving PI (BMI = 31 kg/m2), and 8 HIV-positive patients with diabetes receiving PI (BMI = 34 kg/m2). All patients on PI received indinavir. MEASUREMENTS: Fasting concentrations of glucoregulatory hormones. Direct effects of indinavir (20 microM) on rat pancreatic beta-cell function in vitro. RESULTS: In hyperglycemic HIV-positive subjects, circulating concentrations of insulin, C-peptide, proinsulin, glucagon, and the proinsulin/insulin ratio were increased when compared with those of the other 4 groups (p < .05). Morning fasting serum cortisol concentrations were not different among the 5 groups. Glutamic acid decarboxylase (GAD) antibody titers were uncommon in all groups. High BMI was not always associated with diabetes. In vitro, indinavir did not inhibit proinsulin to insulin conversion or impair glucose-induced secretion of insulin and C-peptide from rat beta-cells. CONCLUSIONS: The pathogenesis of HIV PI-associated diabetes involves peripheral insulin resistance with insulin deficiency relative to hyperglucagonemia and a high BMI. Pancreatic beta-cell function was not impaired by indinavir. HIV PI-associated diabetes mirrors that of non-insulin-dependent diabetes mellitus and impaired insulin action in the periphery.

Hypoglycemia per se stimulates sympathetic neural as well as adrenomedullary activity, but, unlike the adrenomedullary response, the forearm sympathetic neural response is not reduced after recent hypoglycemia.

We tested the hypotheses that 1) hypoglycemia per se stimulates the sympathetic neural as well as the adrenomedullary component of the sympathochromaffin system, and 2) sympathetic neural responses to hypoglycemia, like adrenomedullary responses, are reduced after recent hypoglycemia. To this end, we studied 10 healthy young adults on 2 consecutive days on two separate occasions, on one occasion with euglycemia (5.0 mmol/l) and on the other occasion with hypoglycemia (2.8 mmol/l) from 1000 to 1200 and 1400 to 1600 on day 1 of each occasion. On day 2 of each occasion, plasma epinephrine and norepinephrine (NE) concentrations and rates of systemic NE spillover (SNESO) and forearm NE spillover (FNESO) were measured during hyperinsulinemic (12.0 pmol x kg(-1) x min(-1)) euglycemia (5.0 mmol/l) and hypoglycemia (2.8 mmol/l). Compared with values during euglycemia, plasma epinephrine and NE and rates of SNESO and FNESO all increased during hypoglycemia (P < 0.01). After day 1 hypoglycemia, there were reductions during hypoglycemia on day 2 in plasma epinephrine (2,050 +/- 500 vs. 2,960 +/- 400 pmol/l; P < 0.02), plasma NE (1.35 +/- 0.16 vs. 1.92 +/- 0.20 nmol/l; P < 0.01), and SNESO rates (5.13 +/- 0.84 vs. 6.87 +/- 0.81 nmol/min; P < 0.02). However, FNESO rates were unaltered (1.16 +/- 0.25 vs. 1.27 +/- 0.17 pmol x min(-1) x 100 ml tissue(-1). Thus we conclude that 1) hypoglycemia per se stimulates both the sympathetic neural and adrenomedullary components of the sympathochromaffin system and 2) adrenomedullary, but not forearm sympathetic neural, responses to hypoglycemia are reduced after recent hypoglycemia. The extent to which the lower plasma NE levels and reduced SNESO responses to hypoglycemia after day 1 hypoglycemia reflect reduced NE release from the adrenal medullae, sympathetic nerves other than those in the forearm, or both cannot be determined from these data.

Hypoglycemia is the limiting factor in the management of diabetes.

Hypoglycemia is the limiting factor, both conceptually and in practice, in the management of diabetes mellitus. While the long-term goal of diabetes research must remain the cure and the prevention of the disease and reasonable near-term goals might include perfect insulin replacement or prevention of complications despite ongoing hyperglycemia, the most pressing short-term goal for people with diabetes would seem to be insight leading to strategies that effectively minimize the risk of hypoglycemia and thus permit low-risk glycemic control. Having reviewed the field in detail recently, the author offers his personal views of the key questions - concerning the physiology of glucose counterregulation, its pathophysiology in diabetes, and hypoglycemia in diabetes - that, if answered, might lead to a reduced risk of iatrogenic hypoglycemia in people with diabetes. The overriding question is: How can we learn to replace insulin more perfectly, prevent, correct or compensate for compromised glucose counterregulation, or both?