Practice Guidelines

[Gatekeeper]

Nontraditional Risk Factors May Not Help Assess Coronary Heart Disease Risk

Use of nontraditional risk factors may not help assess coronary heart disease (CHD) risk in asymptomatic men and women with no CHD history, according to a new US Preventive Services Task Force (USPSTF) recommendation statement and accompanying evidence review reported in the October 6 issue of the Annals of Internal Medicine.

The USPSTF found that there was not sufficient evidence to evaluate the balance of benefits vs harms of using any of the 9 nontraditional risk factors to screen asymptomatic men and women with no history of CHD to prevent CHD events.

The 9 nontraditional risk factors evaluated were high-sensitivity C-reactive protein (hs-CRP), ankle-brachial index (ABI), leukocyte count, fasting blood glucose level, periodontal disease, carotid intima-media thickness, coronary artery calcification score on electron-beam computed tomography, homocysteine level, and lipoprotein(a) level.

"...CHD is the most common cause of mortality of adults in the United States," write Ned Calonge, MD, MPH, and USPSTF colleagues from the Agency for Healthcare Research and Quality in Rockville, Maryland. "Treatment to prevent CHD events by modifying risk factors is currently based on the Framingham risk model, which sorts individuals into low-, intermediate-, or high-risk groups. If the risk model could be improved, treatment might be better targeted, thereby maximizing screening benefits and minimizing harms."

The statement authors note that the best opportunity for nontraditional, or novel, risk factors to improve risk classification would be to change those in the intermediate-risk Framingham group to either a low-risk or high-risk group. In the United States, approximately 23 million people with no history of cardiovascular disease are classified by the Framingham score as intermediate risk, but it is unknown how many of these individuals are actually at high risk and could benefit from more aggressive therapy aiming at risk-factor modification reduction.

The Framingham score, which classifies people based on their projected 10-year risk for a major coronary event, uses 7 traditional risk factors for CHD: age, sex, total blood cholesterol level, high-density lipoprotein cholesterol level, smoking status, systolic blood pressure, and use of antihypertensive medication.

Systematic Reviews Performed

The investigators performed systematic reviews of the literature since 1996 on the 9 proposed nontraditional markers of CHD risk. They used a hierarchic approach in hopes of identifying which of these factors could practically and definitively recategorize individuals determined by their Framingham score to be intermediate risk. If these individuals could be reclassified, using any of the novel risk factors, as either high risk or low risk, outcomes might be improved by aggressively targeting risk factors in those individuals newly classified as high risk.

For 7 of the 9 nontraditional risk factors, evidence was insufficient to estimate the percentage of Framingham intermediate-risk individuals who would be reclassified as low risk or high risk using these factors.

Based on hs-CRP screening, approximately 11% of men classified as Framingham intermediate risk would be reclassified as high risk, and approximately 12% would be reclassified as low risk. Small study samples precluded determination of the effect of hs-CRP screening on risk classification in women.

Based on ABI screening, approximately 10% of women classified as Framingham intermediate risk would be reclassified as high risk, but data are insufficient regarding the effect of ABI screening on risk classification in men. For either hs-CRP or ABI screening, however, there are no data to evaluate whether reclassified individuals would benefit from additional treatments targeting these risk factors.

There was limited evidence to assess the harms of screening with novel risk factors. However, potential harms could include risks inherent in lifelong use of medications without proven benefit and psychological and other harms from being misclassified in a higher-risk category.

"The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of using the nontraditional risk factors studied to screen asymptomatic men and women with no history of CHD to prevent CHD events (I statement)," the recommendation statement authors write. "Clinicians should use the Framingham model to assess CHD risk and to guide risk-based therapy until further evidence is obtained....Because adding nontraditional risk factors to CHD assessment requires additional patient and clinical staff time and effort, routinely screening with nontraditional risk factors could result in lost opportunities for provision of other important health services of proven benefit."

Accompanying Evidence Review

The accompanying evidence review was a summary of 9 systematic reviews of novel risk factors by Mark Helfand, MD, from the Oregon Evidence-Based Practice Center, Veterans Affairs Medical Center, and Oregon Health & Science University in Portland, and colleagues.

"Traditional risk factors do not explain all of the risk for incident...CHD events," the review authors write. "Various new or emerging risk factors have the potential to improve global risk assessment for CHD."

The reviewers searched MEDLINE for relevant English-language articles describing cohort studies of novel CHD risk factors published from 1966 to September 2008. Inclusion criteria were no baseline cardiovascular disease in the participants and adjustment for at least 6 Framingham risk factors.

USPSTF criteria were used to assess methodologic quality of individual studies. For each nontraditional risk factor, overall quality of evidence was examined with a modified version of the Grading of Recommendations, Assessment, Development, and Evaluation framework. The potential clinical usefulness of each factor was determined by use of a set of criteria highlighting the importance of the impact of that factor on restratifying individuals at intermediate risk based on the Framingham score.

There was considerable variability across the risk factors in aggregate quality, availability and validity of the evidence, consistency of the results, and applicability to individuals in the general population classified by the Framingham score as intermediate risk. For most of the novel risk factors, no studies have examined their usefulness for reclassifying individuals at intermediate risk.

Limitations of the review included lack of access to original data, precluding arriving at definite conclusions concerning differences in risk prediction among racial and ethnic groups. Furthermore, the review was not able to highlight within-cohort comparisons of multiple novel risk factors.

"...CRP was the best candidate for use in screening and the most rigorously studied, but evidence that changes in CRP level lead to primary prevention of CHD events is inconclusive," the review authors write. "The current evidence does not support the routine use of any of the 9 risk factors for further risk stratification of intermediate-risk persons."

Conclusions of the USPSTF are not to be construed as official positions of the US government or the Agency for Healthcare Research and Quality. The statement and review authors have disclosed no relevant financial relationships.

Ann Intern Med. 2009;151:474-482, 496-507. Abstract

Additional Resources

More information on heart disease and risk factors is available on the Framingham Heart Study Web site. The risk assessment tool based on the Framingham data to estimate one's 10-year risk of a myocardial infarction or coronary death is also accessible.

Study Highlights

Researchers focused on the usefulness of nontraditional variables in further quantifying the CHD risk for intermediate-risk patients. These patients may benefit most by reclassification into low-risk (no treatment of CHD risk) or high-risk (aggressive treatment) groups.
Nontraditional risk factors assessed included hs-CRP, ABI, leukocyte count, fasting blood glucose level, periodontal disease, carotid intima-media thickness, coronary artery calcification score on electron beam computed tomography, homocysteine level, and lipoprotein(a) level.
The collective research into these nontraditional risk factors was mainly limited by a failure to assess the incremental value of nontraditional risk factors vs more traditional risk assessments.
Furthermore, there was no evidence that risk stratification with any nontraditional risk factor was associated with reduced rates of myocardial infarction or cardiovascular mortality.
Several factors, including periodontal disease, coronary artery calcium scans, and increased carotid intima-media thickness, were independent predictors of CHD. However, these variables were not applied specifically to those patients at intermediate risk for CHD.
Although elevated levels of lipoprotein(a) and homocysteine were predictive of a higher risk for CHD events, no research has examined their predictive value beyond traditional risk calculators.
hs-CRP would help to reclassify approximately 11% of men with an intermediate CHD risk into the high-risk category, and 12% of these men would be reclassified as low risk with hs-CRP testing. However, it is unknown whether treating patients reclassified as high risk based on hs-CRP testing is effective in reducing the risk for CHD events. hs-CRP testing is less well researched among women.
ABI may move 10% of women from the intermediate-risk group for CHD into the high-risk group. However, any similar efficacy of ABI testing among men remains unclear.
No studies have directly measured the potential harms associated with CHD risk testing by use of nontraditional variables. However, long-term preventive treatments with statins and aspirin may be increased if more patients are considered moderate risk or high risk for CHD.
Overall, the USPSTF concludes that there is insufficient evidence to assess the balance of benefits and harms of using nontraditional risk factors to screen for CHD risk among asymptomatic adults.

Clinical Implications

The algorithm by ATP III of the National Cholesterol Education Program calculates patients' 10-year risk for a CHD event using their age, sex, systolic blood pressure, serum total cholesterol level, high-density lipoprotein cholesterol level, and smoking status.
There is insufficient evidence to recommend the routine use of nontraditional variables to screen for CHD risk among asymptomatic adults, according to the USPSTF.

[Gatekeeper]

A new joint statement from a number of professional organizations has identified specific criteria for the clinical diagnosis of the metabolic syndrome, tightening up the definition, which previously differed from one organization to the next [1].

The statement, published online October 5, 2009, in Circulation, includes the participation of the International Diabetes Federation (IDF), the National Heart, Lung, and Blood Institute (NHLBI), the World Heart Federation, the International Atherosclerosis Society, and the American Heart Association (AHA) and is an attempt to eliminate some of the confusion regarding how to identify patients with the syndrome.

"This paper represents an attempt to make the definition global," Dr Robert Eckel (University of Colorado, Denver), one of the authors of the new report, told heartwire . "The IDF definition and the [National Cholesterol Education Program Adult Treatment Panel] ATP III definition have been the two that have been utilized most frequently, and now the different organizations--the IDF, the International Atherosclerosis Society, the NHLBI, and the AHA--have all signed on to a single definition. I think that's a step forward in terms of not continuing to confuse people who are working in this field."

Specifically, the new metabolic-syndrome definition streamlines previous differences related to abdominal obesity as defined by measurements in waist circumference. Substantial disparities existed between the previous IDF and the ATP III definitions of what constituted an excessively large waist circumference, by as much as 8 cm between the two groups, but these have been amended. Now, the criteria for elevated waist circumference are based on population- and country-specific definitions, which, although streamlined, do leave some work to be done, said Eckel.

"The problem that still exists is that regional differences around the world may be substantial in terms of what waist circumference confers additional risk for heart disease and diabetes," he said. "The new definition relies on different geographic regions, or different countries, to drill down into their own databases in terms of relating waist circumference to risk." Eckel noted that the IDF previously considered elevations in waist circumference mandatory when defining metabolic syndrome, although the ATP III did not. Now, waist circumference is just one of five criteria that physicians can use when diagnosing the metabolic syndrome. Patients with three of the five criteria--including elevated waist circumference, elevated triglycerides, reduced high-density lipoprotein (HDL)-cholesterol levels, elevated blood pressure, and elevated fasting-glucose levels--are considered to have the syndrome.

Criteria for Clinical Diagnosis of the Metabolic Syndrome Measure  Categorical cut points 
Elevated waist circumference  Population- and country-specific definitions
Elevated triglycerides (drug treatment for elevated triglycerides is an alternate indicator)  >150 mg/dL
Reduced HDL cholesterol (drug treatment for reduced HDL cholesterol is an alternate indicator)  <40 mg/dL for males and <50 mg/dL for females
Elevated blood pressure (drug treatment for elevated blood pressure is an alternate indicator)  Systolic >130 mm Hg and/or diastolic >85 mm Hg
Elevated fasting glucose (drug treatment for elevated glucose is an alternate indicator)  >100 mg/dL


Notably absent from the joint statement is the American Diabetes Association. As reported by heartwire , there are unresolved scientific issues between the ADA and other associations, including the AHA, regarding the metabolic syndrome. Specifically, the ADA, as well as the European Association for the Study of Diabetes (EASD), objected to the manner in which the metabolic syndrome was characterized as a risk factor for heart disease or diabetes, arguing that there was no need to diagnose a patient with the syndrome because emphasis should be placed on aggressively treating the individual risk factors. In 2005, the ADA and EASD issued their own joint statement calling for a critical appraisal of the metabolic syndrome, its designation as a syndrome, and its clinical utility.

To heartwire , Eckel said the IDF, AHA, NHLBI, and others began working on the new metabolic syndrome definition in 2008 and that they simply went ahead without ADA participation. He stressed the metabolic syndrome is not a disease but simply a clustering of risk factors. The original intention of identifying the syndrome was simply to draw clinicians' and the public's attention to the importance of a high-quality lifestyle, and the metabolic syndrome is never meant to be used as a predictor of heart disease or diabetes risk.

References

Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome. A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009; 120:1640-1645. Abstract

Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος

[Raptor]

 The International Diabetes Federation (IDF) announced the release of several new guidelines related to diabetes management here at the IDF 20th World Diabetes Congress. These include the first-ever international guidelines on the management of diabetes in pregnancy and guidelines on the use of self-monitoring of blood glucose (SMBG) among type 2 diabetic patients not being treated with insulin.

Pregnancy and Diabetes Guidelines Call for Universal Screening

Lois Jovanovič, MD, CEO and chief scientific officer of Sansum Diabetes Research Institute in Santa Barbara, California, and clinical professor of medicine at the University of Southern California-Los Angeles Medical Center, is one of the authors of the IDF Global Guideline on Pregnancy and Diabetes. "The guidelines were created with evidence-based medicine. Then we asked an international group [of experts] to give us their opinion," she told Medscape Diabetes & Endocrinology.

"There was no international standard [for the diagnosis and management of gestational diabetes], said Dr. Jovanovič. "There was no consensus, there was a lot of confusion, women were suffering, and their pregnancy outcome was affected by having no standard by which to judge whether their diabetes was worth treating or not. This is the first time there is a worldwide consensus."

A key message of the new guidelines, according to Dr. Jovanovič, is the importance of universal screening. "Look for hyperglycemia in pregnancy," she said. "Preconceptional counseling [also] has to be universal. . . . For a [primary care] physician who has a [patient] in child-bearing years, the first question should be: Are you interested in getting pregnant again?"

Self-Monitoring of Blood Glucose in Noninsulin-Treated Type 2 Diabetes

The IDF Guideline on Self-Monitoring of Blood Glucose in Non-Insulin Treated Type 2 Diabetes was developed in a manner similar to the IDF pregnancy guidelines. Their highlights include the following:

SMBG should be considered at the time of diagnosis but should only be used when patients, their caregivers, and/or their healthcare providers have the knowledge and willingness to incorporate findings into the diabetes management plan.
SMBG should be considered a part of ongoing diabetes self-management education.
SMBG protocols should be individualized.
Patients and their healthcare providers should agree on how to use SMBG data.
Tools used to measure SMBG must be easy to use and accurate.
Unique Features of Guidelines

Both sets of guidelines have key features that differentiate them from guidelines on the same topics put out by other diabetes associations, such as the American Diabetes Association (ADA), said Dr. Jovanovič.

"The ADA hopefully will change soon, but right now they don't subscribe to the philosophy of universal screening [in pregnancy]. They talk about selective screening. Our guidelines not only talk about universal screening but almost assume that every woman has diabetes [and] doing the testing is to reassure her that she doesn't. So, it's a paradigm shift. The second major difference is the [IDF] recommendation that it be a 1-step [oral glucose tolerance] test, not a 2-step test [as currently recommended by the ADA]. The ADA also have the criteria for diagnosis [of gestational diabetes] very high to minimize the number of women identified. The strategies in the [IDF] guidelines actually increase the number of women that would be identified and therefore offer treatment worldwide with 1 standard of care."

According to a coauthor of the SMBG guidelines, David Owens, MD, from the Cardiff University Diabetes Research Unit in the United Kingdom, a unique feature of the IDF SMBG guidelines is that they clarify the role of SMBG in diabetic patients who are not receiving insulin therapy. "For the noninsulin-treated individuals, [other guidelines] say that it's a good idea to incorporate SMBG, . . . but there is no real clarity as to what to do about it. That's where we've tried to extend the story more toward what the patient can do about it in their circumstances. . . . There are [other] guidelines that suggest that maybe there's no reason to monitor blood glucose in the noninsulin-treated, and they say that . . . you need to look at the current evidence and see its limitations. Many of those publications are really not designed to ask [that] question."

[Raptor]

A technology appraisal recommends (QRG) that prasugrel (Efient®) is an option in combination with aspirin for patients who are treated by percutaneous coronary intervention following an acute coronary syndrome. This applies only when they have had a ST-segment-elevation myocardial infarction (STEMI), have had a blocked stent while on treatment with clopidogrel or have diabetes. The Summary of Product Characteristics recommends treatment continues for up to 12 months unless discontinuation is clinically indicated at an earlier time, perhaps due to side effects.

[πρώτη & καλύτερη]

Από το Medscape


•   Taking drug holidays or using intermittent dosing may be strategies to reduce the risks associated with NSAID use.
•   Dyspepsia and GI discomfort occur in 10% to 20% of persons taking NSAIDs, but dyspeptic symptoms do not correlate well with clinically significant ulcers.
•   GI adverse effects are increased with age and comorbidity.
•   The 1-year risk of serious GI bleeding from long-term NSAID use ranges from 1 in 2100 adults younger than 45 years to 1 in 110 older than 75 years.
•   Risk for death for the 2 groups ranges from 1 in 12,353 to 1 in 647 adults, respectively.
•   Concomitant anticoagulant use increases the risk by 5 to 6 times.
•   In those with a history of bleeding ulcers, the risk is 5% in 6 months, even with the use of COX-2 inhibitors or nonselective NSAIDs with a PPI.
•   Eradication of Helicobacter pylori only minimally decreases the rate of peptic ulcer in persons taking NSAIDs.
•   Taking misoprostol with an NSAID reduces ulcer-related complications but is contraindicated in pregnancy (category X) and has undesirable GI effects.
•   Use of PPIs or double-dose antihistamines with NSAIDs decreases the rate of endoscopically diagnosed ulcers.
•   Although low-dose aspirin has been shown to reduce the risk for coronary artery and cerebrovascular disease, other NSAIDs are associated with an increased risk for worsening congestive heart failure, increased blood pressure, and adverse cardiovascular events.
•   Blood pressure increases by 5 mm Hg, whereas use of nonselective NSAIDs and some COX-2 inhibitors also increases blood pressure.
•   COX-2 inhibitors have been implicated in the risk for myocardial infarction, although celecoxib may be safer than the others.
•   COX-2 inhibitors should be avoided in persons at risk for cardiovascular events, who should consider a nonselective NSAID with misoprostol or a PPI for GI protection instead.
•   Sulindac and diclofenac are associated with a higher rate of hepatic dysfunction than other NSAIDs, but clinically significant events are rare.
•   Idiosyncratic liver toxicity may occur in those with hepatitis C or underlying liver impairment.
•   NSAIDs should be avoided in persons with preexisting renal disease, congestive heart failure, or cirrhosis to prevent renal failure.
•   It is unclear whether monitoring renal function in those with renal risk who are taking NSAIDs reduces morbidity or mortality rates.
•   In high-risk persons with recent myocardial infarction or stent placement, aspirin should be continued before and after surgery.
•   In those with bleeding risk, aspirin and other NSAIDs may be withheld before surgery for 5 elimination half-lives (eg, 7 - 10 days before surgery for aspirin and 2 days for ibuprofen).
•   Aspirin should be avoided in those for whom benefits do not outweigh risks.
•   In persons taking anticoagulants, INR monitoring is required when using NSAIDs, and GI prophylaxis should be prescribed.
•   Central nervous system effects are rare and occur mainly in elderly persons, including tinnitus, cognitive changes, confusion, and depression.
•   Indomethacin has been associated with psychosis, whereas aseptic meningitis has been seen with lupus in those taking ibuprofen or naproxen.
•   Bronchoconstriction has been associated with NSAID use, especially in those with underlying respiratory disease such as asthma.
•   NSAIDs are not teratogenic in humans, and the American Academy of Pediatrics considers ibuprofen, indomethacin, and naproxen safe in breast-feeding women.
•   NSAID use close to term in pregnant women is associated with prolonged labor or gestation, blood loss and anemia, and increased risk of neonatal bleeding.
•   Low-dose aspirin is considered safe during pregnancy and lactation.

   Clinical Implications
•   The risk of GI bleeding with NSAID use is increased with age, duration of use, comorbidities, anticoagulant use, and a history of bleeding ulcers.
•   Other systemic adverse effects associated with NSAID use include those affecting the cardiovascular, hepatic, renal, hematologic, nervous, hematologic, and respiratory systems.

[Argirios Argiriou]

Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος

[Argirios Argiriou]

Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος

Στα παραπάνω guidelines στη σελίδα 43 γράφει :
…………
…………………………
Many clinicians have used CT because of lack of access to MR but availability of MR is now improving rapidly across the U.K. Brain scanning may be used to detect stroke mimic (e.g. tumour) but yields are low, unless there are suggestive clinical features. Although CT is very sensitive to haemorrhage early after the event, bleeds may be missed if scanning is delayed.  Brain imaging is of value in determining the presence of vascular lesions (which may be helpful if there is diagnostic doubt) and helping to establish vascular territory where this is not clear. MR scanning, especially with diffusion – weighted imaging / fluid – attenuated inversion recovery (DWI/FLAIR) performed early (ideally within 24 hours) has high sensitivity for the detection of small ischaemic lesions which may be missed on CT-scan.
The clinical question to be addressed is in those patients with TIA who require brain imaging whether MR or CT provides the most information to guide treatment.
……………………
………………………………….
Ποιες απεικονιστικές μεθόδους χρησιμοποιούμε στα Ελληνικά Νοσοκομεία σε περιπτώσεις εγκεφαλικών επεισοδίων;

Πώς λέγεται στα Ελληνικά τo MR scanning, with diffusion – weighted imaging / fluid – attenuated inversion recovery (DWI/FLAIR); Χρησιμοποιούμε απλώς τον Αγγλικό όρο;

Στα παραπάνω guidelines, στον αλγόριθμο της σελίδας 15, γίνεται λόγος σε ορισμένες περιπτώσεις και για θρομβόλυση σε περίπτωση ισχαιμικών εγκεφαλικών.
Εφαρμόζεται θρομβόλυση σε περιπτώσεις ισχαιμικών εγκεφαλικών πουθενά στην Ελλάδα;

[πρώτη & καλύτερη]

περιμένοντας το flone να σχολιάσει.....

Πρακτικές οδηγίες θεραπείας ελαφρού και σοβαρού εγκαύματος, που αλλάζουν κάποιες "πρακτικές" γνώσεις, εδώ Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος

[flone]

Το απόσπασμα που παραθέτει ο κ. Αργυρίου αναφέρεται στην απεικονιστική διερεύνηση παροδικών επεισοδίων εστιακού νευρολογικού ελλείμματος. Αν δεν υπάρχει άλλη εξήγηση, θεωρούνται ισχαιμικής αιτιολογίας, τα γνωστά σε όλους μας "παροδικά ισχαιμικά".

Η αντιμετώπιση των "εγκεφαλικών" στην Ελλάδα γενικότερα, και ειδικά στα "επαρχιακά" νοσοκομεία και ΚΥ βρίσκεται στην εποχή του λίθου.
Πείτε ότι ΔΕΝ σας έχει τύχει να διώξετε σπίτι άνθρωπο που σας έρχεται επειδή πριν μια ώρα και για πέντε λεπτά "μούδιασε" το χέρι του και τώρα δεν έχει τίποτα και σας βγάζω το καπέλο υποκλινόμενος. Για άλλη μια φορά δίνεται η ευκαιρία να φωνάξουμε ότι ΤΑ ΠΑΡΟΔΙΚΑ ΕΠΕΙΣΟΔΙΑ ΔΕΝ ΕΙΝΑΙ "ΕΛΑΦΡΙΑ" ΑΕΕ.

Αν είχατε ασθενή με παροδικό και του κάνατε αξονική (τεχνική νευροαπεικόνισης που ΔΕΝ χρησιμοποιείται διεθνώς παρά μόνο σε 1. κλειστοφοβία 2. βηματοδότη 3. κώμα/επείγουσα εξέταση 4. ψάχνοντας για επασβεστώσεις, είναι ωστόσο η κύρια μέθοδος για τα ελληνικά νοσοκομεία), δεν έδειξε τίποτα, και τον στείλατε σπίτι, τότε μπορείτε να ΜΗΝ κοιμάστε ήσυχοι.

Το είχαμε δει και σε κείνα τα περιστατικά, αν θυμάστε τα "Μαθήματα Νευρολογίας στο ΓΝΦ" (ο κ. Νικολάου και οι καρωτίδες του).

2-C [Πρέπει να αποδειχθεί ότι το έμφρακτο είναι σε περιοχή κατανομής προσθίου (καρωτιδικού) συστήματος, (π.χ. δεν είναι στη γέφυρα) αλλιώς ό,τι και να (ξανα)βρούμε πώς θα μιλάμε για "συμπτωματική" καρωτίδα? Η πρώτη αξονική δεν έδειξε τίποτα και μπορεί να μη δείξει ούτε η δεύτερη. Επίσης (το πιστεύετε?) μπορεί να μη μας φωτίσει ούτε η MRI, αν δεν έχουμε (ζητήσουμε) ακολουθία DWI, που απεικονίζει μόνο τις πρόσφατες ισχαιμικές βλάβες. Ψάξτε το εγκεφαλικό στις εικόνες "MRI flair" και "MRI flair 2" που επισυνάπτονται. Βρήκατε πολλά? Ποιο είναι το πρόσφατο, που έδωσε την κλινική εικόνα? Για δείτε τώρα την "DWI". Νά το, νά το!!!]

Προσθέτω άλλο ένα παράδειγμα (flair im.jpg και dwi im.jpg, ίδιος ασθενής) καθώς και μια ακολουθία Τ2 από άλλον ασθενή (t2.jpg)

Η ακολουθία DWI (Diffusion Weighted Imaging) είναι "λειτουργική". Καταγράφονται οι κινήσεις Brown (θυμάστε λίγο φυσική των ρευστών?) των μορίων του νερού. Σε μια περιοχή πρόσφατης ισχαιμίας, λόγω διαταραχής των μεμβρανικών αντλιών εξαιτίας της ισχαιμίας, έχουμε είσοδο νερού στα νευρικά κύτταρα, οι κινήσεις Brown είναι περισσότερες, με αποτέλεσμα να παίρνουμε διαφορετικό σήμα από τα κύτταρα αυτά. Είναι ακριβώς ο μηχανισμός σχηματισμού του κυτταροτοξικού οιδήματος, για το οποίο δίνουμε στα μεγάλα ισχαιμικά έμφρακτα τη γνωστή σε όλους μας μαννιτόλη. Έτσι, η ακολουθία DWI είναι πολύτιμο εργαλείο για να απαντήσουμε δυο βασικές ερωτήσεις:
1. οφείλονται τα συμπτώματα του ασθενούς σε ισχαιμία? (ιδίως όταν δεν προλάβαμε να τον εξετάσουμε όσο τα είχε, και ακόμα, όταν αναφέρονται μόνο αισθητικά συμπτώματα)
2. Στην περιοχή κατανομής ποιου αγγείου βρίσκεται η πρόσφατη ισχαιμική βλάβη?

Η FLAIR είναι μεταγενέστερη της Τ2 (και υπήρχε πριν την DW) και εξασθενεί (attenuation) το υψηλό σήμα του ΕΝΥγρού (fluid) με την τεχνική inversion recovery (που τώρα δεν θυμάμαι να σας πω ακριβώς τι κάνει). Αν δείτε στην Τ2 που επισυνάπτεται, θα καταλάβετε. Αν αναζητάτε παθολογικό σήμα (που θα φαίνεται "άσπρο", δηλ. αυξημένης έντασης) κοντά στο φλοιό (όπως τα μικρά εμβολικά έμφρακτα) ή περικοιλιακά (νόσος λευκής ουσίας ή εν τω βάθει έμφρακτα, τότε δεν θα το βρείτε γιατί και το παρακείμενο ΕΝΥ είναι επίσης άσπρο. Στη FLAIR, που το ΕΝΥ είναι "μαύρο" και η παθολογία εξακολουθεί και φαίνεται "άσπρη" (έχετε δηλαδή καλό contrast), μπορείτε εύκολα να ενοπίσετε παθολογικό σήμα στις περιοχές αυτές και να το μελετήσετε καλύτερα.

Τη FLAIR στα Ελληνικά την λέτε "φλαιρ" και την DWI την λέτε..."DWI" ή "διάχυση" (αν και με αυστηρά κριτήρια φυσικής δεν είναι σωστή η μετάφραση, έτσι έχει επικρατήσει).
Το να την λέτε, είναι εύκολο. Πού θα την βρείτε;
Σε όλους τους μαγνήτες που αγοράστηκαν από τα τέλη της δεκαετίας του 90 και μετά. Επειδή η αναβάθμιση είναι ρουτίνα στον ιδιωτικό τομέα, δεν θα δυσκολευτείτε. Στο ΕΣΥ, πρέπει να ψάξετε.
Αν έχετε καλή επιχειρηματολογία για να την ζητήσετε, κανείς δεν θα την αρνηθεί.
Η FLAIR είναι πιο «ρουτίνα». Θα την έχετε μάλλον χωρίς να την ζητήσετε.

Διάλειμμα για διαφημίσεις και επανέρχομαι...

[Argirios Argiriou]

Flone, να προλάβω να ρωτήσω πριν συνεχίσεις:

Τι σημαίνει T2;

Αν κατάλαβα καλά από το σχόλιό σου , η FLAIR και η DWI είναι δύο διαφορετικά είδη MRI. Πότε πρέπει να επιλέγουμε τη μια και πότε την άλλη μορφή;

[Πατρωνάκης Μάνος]

 

Πείτε ότι ΔΕΝ σας έχει τύχει να διώξετε σπίτι άνθρωπο που σας έρχεται επειδή πριν μια ώρα και για πέντε λεπτά "μούδιασε" το χέρι του
 και τώρα δεν έχει τίποτα και σας βγάζω το καπέλο υποκλινόμενος.

Μπορεί να συμφωνούμε όπως μπορεί και να διαφωνούμε, μα πάμε παρακάτω.

[flone]

Τι σημαίνει T2;

Αν κατάλαβα καλά από το σχόλιό σου , η FLAIR και η DWI είναι δύο διαφορετικά είδη MRI. Πότε πρέπει να επιλέγουμε τη μια και πότε την άλλη μορφή;

     Ο κλινικός γιατρός παραπέμπει έναν ασθενή για MRI με κάποιες κλινικές ενδείξεις και μια κλινική εικόνα και ένα ιστορικό. Με βάση αυτά, ο ακτινολόγος, που οφείλει να γνωρίζει στοιχειώδη νοσολογία του οργάνου που απεικονίζει, θα διαλέξει ποιες «ακολουθίες» (T1, T2, FLAIR κλπ) θα κάνει. Για παράδειγμα, αν ο ασθενής μας κάνει επιληπτικές κρίσεις, θα πάρει (εκτός από τη «ρουτίνα») και ειδικές στεφανιαίες τομές (FLAIR και Τ1 με «σκιαστικό») για να δει τις έσω κροταφικές δομές (ιππόκαμποι). Αν υποψιαζόμαστε σκλήρυνση, πρέπει να πάρει και οβελιαίες Τ2 και FLAIR για να ψάξει για εστίες στο μεσολόβιο. Αν πρόκειται για ασθενή με παροδικό επεισόδιο, πρέπει να κάνει DWI. Συνεπώς, δεν πρόκειται για διαφορετικά είδη MRI, αλλά για διαφορετικές τεχνικές που δεν γίνονται όλες σε όλες τις εξετάσεις. Η εξέταση είναι μία, μαγνητική τομογραφία.
   Επειδή όμως πολλές φορές τα εργαστήρια λειτουργούν μόνο με τεχνικούς κι έρχονται αργότερα οι γιατροί για να γνωματεύσουν τις εξετάσεις, είναι καλό να επικοινωνούμε από πριν με τους υπεύθυνους για να μας κάνουν αυτά που θέλουμε. Για το συγκεκριμένο που συζητάμε, να ζητήσουμε να μας κάνουν DWI (αν δεν την συμπεριλαμβάνουν στο πρωτόκολλό τους).

Στο θέμα των παροδικών και πάλι, αξίζει να ξαναδιαβάσουμε το “Transient Ischemic Attack: A Scientific Statement for Healthcare Professionals From the American Heart Association…” που επισυνάπτει ο Raptor στο Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος, New AHA/ASA Guidelines on TIA Management ("We think a TIA should be treated as an emergency, just like a major stroke").

Διαλέγω 4 σημεία από το paper:
·   30% to 50% of classically defined TIAs show brain injury on diffusion-weighted magnetic resonance (MR) imaging
·   Large cohort and population-based studies reported in the last 5 years have demonstrated a higher risk of early stroke after TIA than generally suspected. Ten percent to 15% of patients have a stroke within 3 months, with half occurring within 48 hours.
·   Often, health professionals and the public consider TIAs benign but regard strokes as serious. These views are incorrect.
·   Ischemic stroke appears to carry a lower short-term risk of subsequent ischemic stroke than TIA, with reported 3-month risks generally ranging from 4% to 8%.

Although CT is very sensitive to haemorrhage early after the event, bleeds may be missed if scanning is delayed.  

Εδώ νομίζω ότι μπερδεύτηκα λίγο.
Η περίπτωση αιμορραγίας που κλασικά η αξονική «πάσχει» είναι η υπαραχνοειδής αιμορραγία (η ευαισθησία πέφτει λίγες ώρες μετά το επεισόδιο) αλλά αφενός αυτή δεν εκδηλώνεται με παροδικά επεισόδια νευρολογικού ελλείμματος (τουλάχιστο μόνο με αυτά), αφετέρου πιθανολογώ ότι το κείμενο αναφέρεται στην περίπτωση μικρής ενδοπαρεγχυματικής αιμορραγίας που όντως θα μπορούσε να εκδηλωθεί με έλλειμμα διάρκειας αρκετών ωρών. Έχω την εντύπωση ότι θα πρέπει να είναι πολύ “delayed” η εξέταση για να μην την δούμε (εκτός κι αν οι συγγραφείς έχουν υπόψη τους τις καθυστερήσεις στα ραντεβού του NHS!)

Από τα αρχικά ερωτήματα του κ. Αργυρίου (Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος), μένει το θέμα θρομβόλυση:

Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος (Θρομβόλυση στα ισχαιμικά ΑΕΕ)

[Μαρία Χόρτη]

Παραθέτω τα κυριότερα σημεία:

The new guideline has a more pronounced emphasis on informed decision-making (IDM) than in the past.
Men should only be screened "after they receive information about the uncertainties, risks, and potential benefits associated with prostate cancer screening," states the document.

Asymptomatic men with at least a 10-year life expectancy should be offered informed decision making about prostate cancer screening.

The age to begin screening is linked to risk:

    * At age 50 years for average-risk men
    * At age 45 years for higher-risk men (African American ethnicity or first-degree relative with prostate cancer before age 65 years)
    * At age 40 years for appreciably higher-risk men (multiple family members diagnosed with prostate cancer before age 65 years)


The "core elements" of the information to be provided to men to assist with their prostate cancer screening decision include the following:

    * Screening with the PSA blood test detects cancer at an earlier stage than if no screening is performed.
    * Prostate cancer screening might be associated with a reduction in the risk of dying from prostate cancer; however, evidence is conflicting.
    * For men whose prostate cancer is detected by screening, it is not currently possible to predict which men are likely to benefit from treatment.
    * Treatment for prostate cancer can lead to urinary, bowel, sexual, and other health problems that can be significant or minimal, permanent or temporary.
    * The PSA and DRE can produce false-positive or false-negative results.
    * Abnormal results from screening with PSA and DRE require prostate biopsies, which can be painful and lead to complications like infection or bleeding.
    * Not all men whose prostate cancer is detected through screening require immediate treatment. Some require periodic blood tests and prostate biopsies to determine the need for future treatment.


# In men who choose to undergo screening, PSA with or without DRE is recommended.

# The recommendations for follow-up depend on PSA level.
# If PSA level is less than 2.5 ng/mL, screening is recommended every 2 years; for levels of 2.5 ng/mL or higher, screening is recommended every year.

# If PSA level is between 2.5 to 4.0 ng/mL, individualized decision making is recommended:
    * Biopsy is recommended for high-risk patients (African American, family history of prostate cancer, increasing age, and an abnormal DRE result).
    * Previous negative biopsy result confers lower risk.

# The traditional PSA threshold level of 4.0 ng/mL is considered reasonable for biopsy, although a true cutoff level has not been determined.

Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος

[Gatekeeper]

National Institute for Health and Clinical Excellence guidance


Chronic heart failure: Αυγουστος 2010

[Gatekeeper]

NICE guideline

Hypertension in pregnancy : 25 August 2010