An intern in the emergency department has been nervously standing behind you for the past ten minutes while you’ve dealt with a barrage of phone calls.
You look to the patient’s cubicle and see a 30 year-old man looking around nervously between taking bites out of a sandwich and texting on his iphone. D-dimers are specific cross-linked fibrin derivatives that are the product of plasmin-mediated fibrinolytic degradation.
The D-dimer assay can be used as a a€?rule outa€? test in the emergency department when the pre-test probability of venous thromboembolism (VTE) is low.
The pre-test probability is best assessed using a clinical prediction guide (CPG), such as the Wells criteria or the revised Geneva score for pulmonary embolism (PE) and the Wells criteria for deep vein thrombosis (DVT). The D-dimer assay can also be used to help diagnose fibrinolytic disorders such as venom-induced consumptive coagulopathy (VICC) and disseminated intravascular coagulation (DIC). The systematic review of 10 studies by Sutherland et al (2008) showed that D-dimer cannot be used as a sole screening tool for acute aortic dissection. A Best Bets review (updated in 2007) suggests that a negative D-dimer test may be able to rival echocardiography in ruling out an atrial thrombus in atrial fibrilation (negative predictive value ~98%), thus allowing cardioversion to be safely performed in the emergency department without the need for further investigation. D-dimer assays can only be used to rule out VTE if the pre-test probability is sufficiently low. The D-dimer assay is more likely to give a positive result in the elderly, limiting the usefulness of the test. Different types of assay are not standardized and have varying sensitivities and specificities, but they generally have high sensitivity and negative predictive value for the presence of thrombus in patients with low pre-test probabilities. The performance characteristics of the available D-dimer assay can affect its use in clinical decision making. Diagnosis of VTE is based on probabilities and balances the risks of further investigation against the risk of missing the diagnosis.
D-dimer negative patients can still develop VTE and should be advised to return if symptoms worsen or new symptoms develop (e.g. At our institution, with a highly sensitive d-dimer, we would still do the d-dimer if the Wells score is 6 or less. Our New BMJ website does not support IE6 please upgrade your browser to the latest version or use alternative browsers suggested below. Note that highly sensitive D-dimer assays can be used to rule out PE in patients with low or intermediate Wells scores (0 to 6), less sensitive assays should only be used for low Wells scores (0 to 2). However many of the studies included were in Japanese and only the English language abstracts were appraised. What situations may result in a ‘false negative’ D-dimer assay when investigating for possible venous thromboembolic disease?
What ‘non-pathological’ conditions are associated with elevated D-dimer titres? However, if the D-dimer is negative it can still be used to rule out VTE in elderly patients with low pre-test probabilities.
The D-dimer result is nearly always positive in the third trimester, and less so the earlier the pregnancy. Potential of an age adjusted D-dimer cut-off value to improve the exclusion of pulmonary embolism in older patients: a retrospective analysis of three large cohorts. D-dimer as the sole screening test for acute aortic dissection: a review of the literature. Derivation of a simple clinical model to categorize patienta€™s probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer.
Key areas of interest include: the ED-ICU interface, toxicology, simulation and the free open-access meducation (FOAM) revolution.
It should only be ordered if the diagnosis of PE is going to be pursued with further investigation if the test is positive.
Our Team, headed by Mike Cadogan & Chris Nickson, consists (mostly) of emergency physicians and intensivists based in Australia and New Zealand. 108 trials studied differences in blood pressure between study drug and placebo (or control group not receiving the study drug) (“blood pressure difference trials”), and 46 trials compared drugs (“drug comparison trials”).


A recent retrospective study by Douma et al (2010) suggests that higher cut-offs might be safely used in patients over 55 years of age. Well, a plain CXR showed a right sided infiltrate and patient was admitted with penicillin. The extra effect was limited to a few years after myocardial infarction, with a risk reduction of 31% compared with 13% in people with CHD with no recent infarct (P=0.04).
Symptoms of high progesterone include: mood swings, breast tenderness, anxiety, and depression. Fortunately the morning after docs wanted to be on the safe side and had a CT which showed a central PE. In the other blood pressure difference trials (excluding CHD events in trials of ? blockers in people with CHD), there was a 22% reduction in CHD events (17% to 27%) and a 41% (33% to 48%) reduction in stroke for a blood pressure reduction of 10 mm Hg systolic or 5 mm Hg diastolic, similar to the reductions of 25% (CHD) and 36% (stroke) expected for the same difference in blood pressure from the cohort study meta-analysis, indicating that the benefit is explained by blood pressure reduction itself. Reducing stress, eating healthier and exercising regularly can help to lower progesterone levels. The percentage reductions in CHD events and stroke were similar in people with and without cardiovascular disease and regardless of blood pressure before treatment (down to 110 mm Hg systolic and 70 mm Hg diastolic). Vaginal dryness, loss of libido, anxiety, depression, oily skin, acne, and weight gain are all potential symptoms of high progesterone.
Combining our results with those from two other studies (the meta-analyses of blood pressure cohort studies and of trials determining the blood pressure lowering effects of drugs according to dose) showed that in people aged 60-69 with a diastolic blood pressure before treatment of 90 mm Hg, three drugs at half standard dose in combination reduced the risk of CHD by an estimated 46% and of stroke by 62%; one drug at standard dose had about half this effect. The present meta-analysis also showed that drugs other than calcium channel blockers (with the exception of non-cardioselective ? blockers) reduced the incidence of heart failure by 24% (19% to 28%) and calcium channel blockers by 19% (6% to 31%).Conclusions With the exception of the extra protective effect of ? blockers given shortly after a myocardial infarction and the minor additional effect of calcium channel blockers in preventing stroke, all the classes of blood pressure lowering drugs have a similar effect in reducing CHD events and stroke for a given reduction in blood pressure so excluding material pleiotropic effects. The proportional reduction in cardiovascular disease events was the same or similar regardless of pretreatment blood pressure and the presence or absence of existing cardiovascular disease. Guidelines on the use of blood pressure lowering drugs can be simplified so that drugs are offered to people with all levels of blood pressure.
Our results indicate the importance of lowering blood pressure in everyone over a certain age, rather than measuring it in everyone and treating it in some.IntroductionDespite the widespread use of blood pressure lowering drugs and the results of many randomised trials,1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 w1-w162 uncertainty remains about which drugs to use and who to treat. Firstly, do ? blockers have a special effect over and above lowering blood pressure in preventing coronary heart disease (CHD) events in people with a history of CHD? We aimed to answer this question from an analysis of all relevant trials, and then to answer four further questions after excluding CHD events in trials of ? blockers in people with a history of CHD if they did have a special effect.
Secondly, does the effect of blood pressure lowering drugs in preventing CHD and stroke differ in people with and without a history of cardiovascular disease (that is, is there a different effect in secondary and primary prevention)? Thirdly, does blood pressure reduction alone explain the effect of blood pressure lowering drugs in preventing CHD and stroke? There are claims of additional non-blood pressure lowering (so called pleiotropic) effects of drugs.7 8 13 w135 w136 w139 Selected trial data have been used to suggest that each of the five main classes of blood pressure lowering drugs (thiazides, ? blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and calcium channel blockers) has a greater preventive effect,1 2 3 4 5 6 7 8 9 10 11 12 13 w126 w129 and each a lesser preventive effect,9 10 11 12 13 14 15 16 17 18 19 20 w126 w135 than other drugs. Clinical guidelines tend to reflect the view that differences in efficacy exist.21 22 23 Fourthly, should the use of blood pressure lowering drugs be limited to people with “high” blood pressure and not given to those at high risk of cardiovascular disease who have a lower blood pressure?
A corollary is whether blood pressure should be reduced to a limited extent only, a treat to target approach.9 10 11 21 22 23 24 Although cohort (prospective observational) studies do not show a lower blood pressure limit below which risk ceases to decline (“the lower the better”),25 26 27 this has not been shown in randomised trials across a wide range of blood pressure. Finally, what is the quantitative effect of taking one or more blood pressure lowering drugs in lowering blood pressure and preventing CHD events and stroke according to dose, pretreatment blood pressure, and age? Limits were Medline publication type “clinical trial” or “controlled clinical trial” or “randomized controlled trial” or “meta-analysis”.
We also searched the Cochrane Collaboration and Web of Science databases and the citations in trials and previous meta-analysis and review articles.We excluded non-randomised trials and trials in which treated groups but not control groups had other interventions as well as blood pressure reduction, such as cholesterol reduction. We excluded trials in patients with chronic renal failure because these patients typically have high blood pressure and high rates of cardiovascular disease and their response to standard blood pressure lowering therapy may differ from other people.
We also excluded trials in which fewer than five CHD events and strokes were recorded or the duration of treatment was less than six months, as these data would contribute little to the overall results and substantially increase the complexity of the analyses. Randomised trials were otherwise included irrespective of participants’ age, disease status, blood pressure before treatment, or use of other drugs.Data extractionWe recorded the numbers of participants having one or more CHD events (defined as fatal or non-fatal myocardial infarction or sudden cardiac death but excluding “silent” infarcts) and one or more strokes (haemorrhagic and ischaemic strokes could not be distinguished). We also recorded the numbers of participants with a new diagnosis of heart failure or an exacerbation of existing heart failure based on new hospital admissions or death from the disorder. Two authors (MRL and NJW) independently recorded data, with differences resolved by discussion.


Outcomes were recorded regardless of whether participants took their allocated tablets (intention to treat analysis). Change in blood pressure in the trials (value on entry minus the average value during the trial in the treated group, minus the same change in the control group) was recorded on an intention to treat basis by determining the numbers of participants in the treated and in the control groups who stopped attending the clinics (so that their blood pressure reduction was no longer recorded) and taking the difference in blood pressure between them to be zero after they left the trial.Categories of trialThe trials were divided into three predefined categories according to whether the recruitment was based on participants having no history of cardiovascular disease, a history of CHD (acute myocardial infarction, coronary artery disease without recent infarction, or heart failure), or a history of stroke (or other cerebrovascular disease).
In the trials of participants with no history of vascular disease, blood pressure was usually high, variably defined, and a treat to target approach was used, typically based on one drug with the dose increased before the addition of other drugs to reach the target blood pressure.
In the trials of participants with a history of CHD there was generally no selection by blood pressure and no blood pressure target; treated patients were allocated a specified drug in fixed dose, varied only to avoid adverse effects. In the trials of participants with a history of stroke most followed the treat to target approach, some followed the specified drug approach. In trials of participants who had acute myocardial infarction on entry sudden deaths while in hospital were not recorded because it was not our objective to assess the efficacy of the drugs in reducing mortality in the period immediately after infarction; the CHD events and heart failure episodes we recorded were either those designated as reinfarction or those occurring after hospital discharge.
Similarly in trials of participants who had heart failure on entry, sudden deaths were not recorded (as ischaemia and worsening heart failure could not be distinguished as causes). Ninety two of the 108 trials in this category were placebo controlled, but in 16 the control group was not given a placebo. Additional blood pressure lowering drugs were commonly used in the different groups in each trial—for example, in trials comparing an angiotensin converting enzyme inhibitor with placebo in people with CHD, participants in both groups might also receive ? blockers or calcium channel blockers, whereas in trials in which a treat to target approach was used, add-on drugs were given if necessary in both actively treated and placebo treated participants to reach their blood pressure targets (the target being lower for treated participants than for placebo participants). Through their design the blood pressure difference trials ensured that the intervention groups were more intensively treated. Although additional drugs could be used in either group there was no intention to achieve a different blood pressure reduction in one group compared with another. These trials therefore tested for effects of a drug that were unrelated to lowering blood pressure.
In two drug comparison trials of three drugsw129 w147 each of the three pairwise comparisons was recorded separately. In both trial categories, additional drugs of a class allocated to one randomised group could not be used in the other.Statistical analysisAll statistical analyses were done using Stata software. We combined relative risk estimates of disease events from individual trials using a random effects model31 (which avoids assuming that participants in the individual trials in the meta-analysis are sampled from populations in which the intervention has the same quantitative effect). If reductions in both systolic and diastolic blood pressures were reported (as in most trials), we took the average of the two risk estimates (more strongly predictive than either alone25).
It also showed that the blood pressure lowering effect of the drugs increased with dose and with pretreatment blood pressure, and reported regression equations that quantified the reduction in blood pressure from one drug according to pretreatment blood pressure. The estimated blood pressure reduction for two or three drugs at standard dose was calculated by applying these equations to each drug in turn, allowing for the effect of the first in lowering pretreatment blood pressure for the second, and the second for the third.
Age specific slopes of the lines (regression coefficients) were published, permitting the calculation of the predicted proportional reduction in disease events for any age and blood pressure difference.
At age 60-69, the relative risk of stroke is 0.43 (57% decrease) for a 20 mm Hg decrease in systolic blood pressure.
The sloping lines in the lower portion of figure 6 reflect these regression coefficients for stroke and CHD events in the age groups 50-59, 60-69, and 70-79 years.The effect of blood pressure lowering drugs in reducing the risk of CHD events and stroke can therefore be estimated according to the reduction in systolic or diastolic blood pressure (or the average of the two), from the regression slope, S, and the decrease in blood pressure, d, from the above equations. Table 1? summarises the trials (see web extra tables 1i-iii and 2 for individual data from the trials).
The greater protective effect of ? blockers in people with CHD was explained by a greater effect in the 27 trials that recruited participants at the time of an acute myocardial infarction (within a month in 25 trials and within four months in the other two).
In these 11 trials about 75% of the participants had had an infarct, but not within the last four months and typically several years before. ? blockers used for one or two years after an acute myocardial infarction were therefore about twice as effective as ? blockers used in other circumstances and about twice as effective as other drugs used in any circumstances (see web figures 1a-e for forest plots of the individual trial results).Fig 1?Relative risk estimates of coronary heart disease events in single drug blood pressure difference trials according to drug (? blockers or other), presence of CHD, and for ? blockers according to acute myocardial infarction on entry.



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Comments

  1. 10.07.2015 at 14:50:55


    Cannot be taken out and used.

    Author: Die_Hard
  2. 10.07.2015 at 21:33:47


    You used to ??including perhaps needing to get up every couple of hours during (low blood sugar.

    Author: APT
  3. 10.07.2015 at 13:47:30


    Are blood glucose meters and brain tumors that.

    Author: HsN