Indeed, no single symptom or sign or combination of clinical findings is specific to pulmonary thromboembolism.
Plasma levels of D-dimer, a degradation product of cross-linked fibrin, are elevated in the presence of thrombus. Using a D-dimer threshold between 300 and 500 ng/mL, the quantitative enzyme-linked immunosorbent assay (ELISA) has shown a sensitivity for venous thromboembolism of 97% and a specificity of 45%. Therefore, the absence of D-dimer using the ELISA assay provides strong evidence against venous thromboembolism. Two considerations have delayed widespread inclusion of plasma D-dimer assays into diagnostic algorithms. First, the accurate quantitative ELISA assay used in multiple studies takes several hours to perform and is not widely available. Commonly used latex agglutination assays are much less sensitive and are difficult to standardize. Second, the D-dimer is elevated in most hospitalized patients, particularly those with malignancies or following surgery. Appropriate diagnostic thresholds are not yet established for inpatients.
Chest radiography—The chest radiograph is necessary to exclude other common lung diseases and to permit interpretation of the ventilation-perfusion scan, but it does not establish the diagnosis by itself. The chest radiograph was normal in only 12% of patients with confirmed pulmonary thromboembolism in the PIOPED study. The most frequent findings were atelectasis, parenchymal infiltrates, and pleural effusions. However, the prevalence of these findings was the same in hospitalized patients without pulmonary thromboembolism. A prominent central pulmonary artery with local oligemia (Westermark's sign) or pleural-based areas of increased opacity that represent intraparenchymal hemorrhage (Hampton's hump) are uncommon. Paradoxically, the chest radiograph may be most helpful when normal in the setting of hypoxemia.
Lung scanning—A perfusion scan is performed by injecting radiolabeled microaggregated albumin into the venous system, allowing the particles to embolize to the pulmonary capillary bed. To perform a ventilation scan, the patient breathes a radioactive gas or aerosol while the distribution of radioactivity in the lungs is recorded.
A defect on perfusion scanning represents diminished blood flow to that region of the lung. This finding is not specific for pulmonary embolism. Defects in the perfusion scan are interpreted in conjunction with the ventilation scan to give a high, low, or intermediate (indeterminate) probability that pulmonary thromboembolism is the cause of the abnormalities. Criteria for the combined interpretation of ventilation and perfusion scans (commonly referred to as a single test, the V/Q scan) are complex, confusing, and not completely standardized. A normal perfusion scan excludes the diagnosis of clinically significant pulmonary thromboembolism (negative predictive value of 91% in the PIOPED study). A high-probability V/Q scan is most often defined as having two or more segmental perfusion defects in the presence of normal ventilation and is sufficient to make the diagnosis of pulmonary thromboembolism in most instances (positive predictive value of 88% among PIOPED patients). In the presence of abnormal pulmonary vasculature, as commonly happens in prior pulmonary thromboembolism, or if the clinical pretest probability for embolism is low, angiography may be indicated even in the presence of a high-probability V/Q scan.
Ventilation-perfusion scans are most helpful when they are either normal or indicate a high probability of pulmonary thromboembolism. Such readings are reliable—interobserver agreement is best for normal and high-probability scans, and they carry predictive power. The likelihood ratios associated with normal and high-probability scans are 0.10 and 18, respectively, indicating significant and frequently conclusive changes from pretest to posttest probability.
However, 75% of PIOPED V/Q scans were nondiagnostic, ie, of low or intermediate probability. At angiography, these patients had an overall incidence of pulmonary thromboembolism of 14% and 30%, respectively. The likelihood ratios associated with low-probability and intermediate scans are 0.36 and 1.2, respectively, confirming the clinical impression that these studies add little diagnostic information. One of the most important findings of PIOPED was that the clinical assessment of pretest probability could be used to aid the interpretation of the V/Q scan. For those patients with low-probability V/Q scans and a low (20% or less) clinical pretest probability of pulmonary thromboembolism, the diagnosis was confirmed in only 4%. Such patients may reasonably be observed without angiography. All other patients with nondiagnostic V/Q scans require further testing to determine the presence of venous thromboembolism.
The integrated approach uses the clinical likelihood of venous thromboembolism along with the overlapping results of noninvasive testing to come to one of three decision points: to establish venous thromboembolism (pulmonary thromboembolism or DVT) as the diagnosis; to exclude venous thromboembolism with sufficient confidence to follow the patient without therapy; or to refer the patient for pulmonary angiography. An ideal diagnostic algorithm would proceed in a stepwise fashion to come to these decision points in a cost-effective way at minimal risk to the patient.
The most innovative developments in systematic diagnosis have suggested three changes to this standard model. First are attempts to refine the clinical pretest probability to identify a subset of patients at low likelihood for venous thromboembolism. Second, some investigators have used negative D-dimer determinations (to exclude venous thromboembolism) in combination with venous ultrasonography (to establish the diagnosis of DVT) to evaluate a majority of outpatients before proceeding to ventilation-perfusion scanning. The increasing availability of improved and rapid D-dimer assays may result in significant changes to these algorithms in the future. Third, there is active debate about the role of spiral CT in the initial evaluation of suspected pulmonary thromboembolism; clarification should come from studies using multi-detector-row spiral CT scanners.
durere de cap wrote:un copil (16 ani) se prezinta cu icter.i se fac toate analizele din care rezulta ca nu are hepatita; are doar bilirubina directa dubla si cea indirecta tripla.I se recomanda Liv52 si Fenobarbital timp de 3 luni.
Intre timp il trimite la centrul de hematologie unde-i fac electroforeza Hb unde nu are nimic Hb.
Doctora care l-a urmarit sustine ca nu are Sdr. Gilbert, ci ca-i lipseste o enzima,dar nu stie care si ca ar fi bine daca s-ar duce la spitalul Fundeni,la dr. Irinel Popescu.
Mentionez faptul ca dupa 6 luni de tratament cu cele mentionate mai sus copilul are cele 2 bilirubine triple si LDH-ul este scazut. Inainte sa-i apara icterul l-a durut ficatul, splina si piciorul drept.Acum are doar o stare de somnolenta permanenta,dar nu-l doare nimic.
Poate e cineva care poate sa-mi dea un sfat s-o linistesc pe mama lui, care crede ca are si el SLA, ca tatal lui (consider ca e aberant!).
Users browsing this forum: No registered users and 19 guests
, ca sa zic asa. Prompti baietii aia, n-am nimic de zis. 
