Pulmonary embolism (PE), and pulmonary embolism (PE), is a closure of one or more pulmonary artery by thrombus, which are derived from other regions of the body, typically in the large veins of the legs or of the basin. Risk factors of pulmonary embolism are diseases that impede venous return, diseases that lead to Endothelverletzungen OR MALFUNCTION, and underlying thrombophilia. The symptoms of pulmonary embolism are nonspecific and include dyspnea, pleuritic chest pain and in severe cases, dizziness, syncope, syncope or heart and lung failure. The study findings are also nonspecific and may tachypnea, tachycardia, and in more severe cases take Hypotonieum. The diagnosis of a pulmonary embolism is provided by CT angiography, ventilation / perfusion scintigraphy or occasionally angiography of the pulmonary arteries. The treatment of pulmonary embolism with anticoagulants and sometimes clot lysis with thrombolytics or surgical removal. If anticoagulation is contraindicated, a V. cava inferior filter should be placed. Preventive measures include anticoagulants and / or sometimes mechanical compressing aids that are attached to the legs of hospital patients.
Pulmonary embolism affects an estimated 117 people per 100,000 person-years, resulting in approximately 350,000 cases per year (probably at least 100,000 in the US) may occur up to 85,000 deaths annually and away. It mainly affects adults.
Pulmonary embolism (PE), and pulmonary embolism (PE), is a closure of one or more pulmonary artery by thrombus, which are derived from other regions of the body, typically in the large veins of the legs or of the basin. Risk factors of pulmonary embolism are diseases that impede venous return, diseases that lead to Endothelverletzungen OR MALFUNCTION, and underlying thrombophilia. The symptoms of pulmonary embolism are nonspecific and include dyspnea, pleuritic chest pain and in severe cases, dizziness, syncope, syncope or heart and lung failure. The study findings are also nonspecific and may tachypnea, tachycardia, and in more severe cases take Hypotonieum. The diagnosis of a pulmonary embolism is provided by CT angiography, ventilation / perfusion scintigraphy or occasionally angiography of the pulmonary arteries. The treatment of pulmonary embolism with anticoagulants and sometimes clot lysis with thrombolytics or surgical removal. If anticoagulation is contraindicated, a V. cava inferior filter should be placed. Preventive measures include anticoagulants and / or sometimes mechanical compressing aids that are attached to the legs of hospital patients. Pulmonary embolism affects an estimated 117 people per 100,000 person-years, resulting in approximately 350,000 cases per year (probably at least 100,000 in the US) may occur up to 85,000 deaths annually and away. It mainly affects adults. Etiology Almost all pulmonary emboli arise from thrombi in the veins of the legs or the Beckensn (deep vein thrombosis). The risk of embolization is higher proximally with thrombus of the calf veins. Thromboembolism may also consist of the arm veins or the central vein of the pelvis come (caused by central venous catheters or thoracic outlet syndrome). Risk factors for deep vein thrombosis and pulmonary embolism (see Table: Risk factors for deep vein thrombosis and pulmonary embolism) are the same in children and adults and include Factors affecting venous return, including bed rest and Belllägerigkeit without motion factors that cause endothelial injury or dysfunction Underlying hypercoagulability (thrombophilia) disease control risk factors for deep vein thrombosis and pulmonary embolism age of> 60 years cancer Hormonal modulation estr ogen receptor modulators (eg. As raloxifene, tamoxifen) Exogenous estrogens and progestogens, including oral contraceptives and estrogen therapy Exogenous testosterone heart failure immobilization indwelling catheters myeloproliferative diseases (hyperviscosity) nephrotic syndrome obesity Pregnancy / Postparta lzeit Earlier thromboembolism sickle cell anemia smoking stroke Thrombotic disorders (thrombophilia) antiphospholipid antibody syndrome antithrombin III deficiency Factor V Leiden (activated protein C resistance) heparin-induced thrombocytopenia, hereditary disorders of fibrinolysis hyperhomocysteinemia increase in Factor VIII values ??increase in factor XI levels increase in off-Will eBrand-factor values ??paroxysmal nocturnal hemoglobinuria Protein C deficiency Protein S deficiency prothrombin G20210A Genvariant deficiency or impaired function of the tissue factor pathway inhibitor trauma / surgery Other factors that are associated with reduced mobility, vein damage or hypercoagulability. Pathophysiology has a deep vein thrombosis developed so emboli can dislodge and travel through the venous system and the right side of the heart into the pulmonary arteries, where they close one or more vessels partially or completely. The consequences depend on size and number of emboli, the Constitution of the lung underlying how well the right ventricle (RV) function and the ability of the intrinsic fibrinolytic system to dissolve the emboli again. Death occurs by right heart failure. Small emboli can no acute physiological effects remain and many begin immediately dissolve again and disappeared again within hours or days. Larger emboli can reflexly an increase in ventilation (tachypnea), hypoxemia due to ventilation / perfusion (V / Q) -Missverhältnisses and Oxygen deficiency in the blood due to heart failure, atelectasis by alveolar hypocapnia and Surfactantstörungen, and an increase in pulmonary vascular resistance by mechanical cause obstruction and vasoconstriction. By endogenous fibrinolysis, most emboli resolve, even of medium size, on and physiological changes disappear within hours or days. Some emboli can not be degraded by endogenous fibrinolysis, they can stay and build exist. A LE may be referred to as a solid, depending on the physiological effects: Impaired right ventricular function with hypotension as systolic BP & lt defined; 90 mm Hg or a drop in systolic BP of ? 40 mm Hg from baseline for a period of 15 min and predicts a significant risk of death within hours or days Submassiv: Impaired right ventricular function without hypotension Low: The lack of right heart function and absence hypotension a saddle embolism describes a pulmonary embolism, which is located in the fork of the main pulmonary artery and in the right and left pulmonary artery; Saddle embolism submassiv or solid generally. In 3 to 4% of cases the residual chronic obstruction caused pulmonary arterial hypertension (chronic thromboembolic pulmonary hypertension), which develops over months to years and may lead to chronic right heart failure. If larger emboli close the large pulmonary arteries, or if many smaller emboli occlude> 50% of the other distal arterial system, then increases the right ventricular pressure and can lead to acute RV failure, shock or sudden death. The mortality risk depends on the extent and the speed of the right cardiac pressure increase and the underlying cardiopulmonary status of the patient. Patients with pre-existing pulmonary disease have a higher mortality risk, but young and / or otherwise healthy patients can survive LE, which closes> 50% of the pulmonary vascular bed. (Represented interruption of the pulmonary artery blood flow, which leads to necrosis of the lung tissue, and sometimes [peripherally situated] by a pleural based often wedge-shaped pattern on the chest x-ray [Hampton hump] or other imaging method), pulmonary infarction occurs in <10% of patients with diagnosed pulmonary embolism. This low rate is to the dual blood supply to the lung (i. E. Bronchial and pulmonary) recycled. In general, a pulmonary infarction occurs because of small emboli sitting in more distal pulmonary arteries. LE can also be non-thrombotic. Symptoms and complaints Many pulmonary emboli are not relevant to a minor degree, pathophysiological and asymptomatic. Even if symptoms are present, they are non-specific and vary in frequency and intensity, depending on the extent of pulmonary vascular closure and pre-existing cardiopulmonary dysfunction. Emboli often cause acute dyspnea Pleuritic chest pain dyspnea may be minimal at rest and worsen with activity. Less common symptoms cough hemoptysis When an elderly patient the first symptom may be a altered mental status. Extensive LE can h in hypotension, tachycardia, dizziness / syncope, syncope or cardiac arrest manifest. The most common symptoms of PE include tachycardia and tachypnea. Tachycardia tachypnea rare patients have hypotension, a through increased Pulmonalisanteil (P2) caused denominated second heart sound (S2), and moist RG or wheezing. In the presence of right heart failure distended neck veins and are visible after shifted RV RV and a gallop rhythm (third heart sound [S3) with or without tricuspid regurgitation may be audible. Fever, if present, is usually low unless it is caused by an underlying disease. Typical characteristics of pulmonary infarcts are chest pain (mainly pleuritisch), and occasionally hemoptysis. Chronic thromboembolic pulmonary hypertension causes symptoms and complaints of right heart failure including dyspnea on exertion, rapid fatigue and peripheral edema, which form inside of months and years. Patients with acute LE may also have symptoms of deep vein thrombosis (i. E., Pain, swelling and / or erythema of a leg or an arm). Although such symptoms are often absent in the legs. Diagnosis Profound suspected assessment of pretest probability (include based on clinical findings, pulse oximetry and X-rays of the chest) Subsequent tests based on pretest probability The diagnosis is challenging because the symptoms and complaints are nonspecific and the diagnostic tests not 1,005 sensitive and are specific. It is important to involve the LE in the differential diagnosis when non-specific symptoms such as dyspnea, pleuritic chest pain, coughing up blood, dizziness or syncope occur. Therefore, an LE should be considered in the differential diagnosis of the patient into consideration, cardiac ischemia, heart failure exacerbation of COPD pneumothorax pneumonia sepsis acute chest syndrome have Acute anxiety disorder with hyperventilation (in patients with sickle cell anemia). Significant, unexplained tachycardia may indicate. LE should also be considered in any elderly patients with tachypnea, and altered mental status. The initial diagnosis should include pulse oximetry and a radiograph of the chest. ECG, ABG, or both can help to exclude other diagnoses (e.g. acute myocardial infarction). The radiograph of the chest is usually non-specific, but can show atelectasis, focal infiltrates, a superscript diaphragm or pleural effusions. The classic radiological findings as focal loss of vascular pattern (Westermark sign), peripheral wedge-shaped opacity (Hampton hump), or widening of the right descending pulmonary artery (Palla characters) have a LAE suspect but are unusual (ie insensitive) and have a unknown specificity. Radiographs of the chest can also help rule out pneumonia. An error caused by a pulmonary embolism pulmonary infarction may be confused with pneumonia. The pulse oximetry provides a quick method to determine the oxygenation (editor's note, however, Red .: More meaningful is the BGA, under which the compensatory mechanisms of the body [usually hypoxemia despite hyperventilation with hypocapnia] can be judged...); a symptom of LE is the hypoxemia, and it is further investigation necessary. The BGA-measurement can be increased alveolar to arterial oxygen saturation (A-a) difference (sometimes called A.G gradient) show or hypocapnia, one or both of these tests are moderately sensitive to LE, but not specific. BGA testing should be considered, especially for patients with dyspnea or tachypnea, where no hypoxemia was found with pulse oximetry. The oxygen saturation may be normal due to a load through a small blood clots or by hyperventilation compensation; very low, detected with ABG measurement pCO2 can confirm a hyperventilation. Clinical Calculator: A-a gradient in the ECG is most common to find a tachycardia, occasionally various ST segment changes that are specific to a LE are not (An ECG in pulmonary embolism.). A S1Q3T3 type or a new onset right bundle branch block may be the expression of a conduction disturbance by the rapid pressure increase in the RV; these findings are overly specific, but insensitive, and occur in only about 5% of patients. Further variations of the heart axis to the right (R> S in V1) and a P may occur pulmonary. T-wave inversion in leads V1 to V4 can also occur. An ECG in pulmonary embolism. The ECG shows sinus tachycardia at a rate of 110 beats / min, a S1Q3T3 and R = S in V1 in a patient with proven acute lung embolism. Clinical Probability The clinical probability of the existence of a LE can be determined by the combination of ECG and chest X-ray findings with the medical history and physical examination findings. Clinical prediction scores, such as the Wells score, the revised Geneva score or Pulmonary Embolism Rule-out Criteria (PERC) score, can help if an acute PE is present doctors in assessing the probability. These systems refer to a variety of clinical factors with cumulative scores that correspond to the terms of the probability of pulmonary embolism before the test (pretest probability). For example, the result of the Wells score is classified as likely or unlikely for a pulmonary embolism. However, the judgment whether LE is more likely than an alternative diagnosis is somewhat subjective. The clinical judgment of experienced doctors may also be accurate or more accurate than the results of such prediction scores. LE should probably be viewed as likely one or more symptoms and complaints, particularly dyspnea, hemoptysis, tachycardia, or hypoxia, can not be explained clinically or by the results of X-ray examination of the chest. The pretest probability directs the testing strategy and interpretation of test results. In patients with a low clinical probability LE probably only a few additional studies necessary (ie, D-dimer test) In such cases, a negative D-dimer test shows (<0.4 ug / ml) significantly, the absence of a pulmonary embolism , If there is a high clinical suspicion of a LE and the bleeding risk is low, the patient will be given directly anticoagulants, while the diagnosis is confirmed by additional tests. Clinical Calculator: probability of DVT: Wells Score System Diagnostic tests screening with D-dimer in order to check whether the pretest probability is unlikely. When the pretest probability is likely or if the D-dimer result is increased, CT angiography or V / Q scan when CT contrast is contraindicated. (To avoid eg. As to lung imaging) sometimes ultrasonography of the legs or arms There is no generally accepted algorithm for the approach of acute pulmonary embolism The most useful tests to diagnose an LE or exclude, d-dimer test CT angiography V / Q scintigraphy duplex sonography D-dimers are a by-product of the endogenous fibrinolysis, so that elevated levels are suggestive of the presence of a fresh thrombus. When the pretest probability is considered unlikely, has a negative D-dimer levels (<0.4 ug / ml) most likely due to the absence of a LE down with a negative predictive value of> 95%; in most cases this is a sufficiently reliable result to exclude the diagnosis of LE routinely. However, elevated levels are not specific for venous thrombosis, as many patients have no deep vein thrombosis (DVT) or LE also increased levels and, therefore, further testing is required when the d-dimer levels are elevated, or when the pretest probability of LE is likely. CT angiography is the preferred imaging technique for the diagnosis of acute PE. It is fast, accurate and highly sensitive and specific. There may also be more information on other lung diseases give (z. B. Detection of pneumonia instead of PE as a cause of hypoxia or pleuritic chest pain). Although poor quality of scans due to motion artifacts or poor contrast bolus limit the sensitivity of the investigation have improvements in CT technology acquisition times reduced to less than 2 s and enter relatively motion-free images in patients who are dysponisch. Fast scanning time allow the use of smaller amounts of iodinated contrast agents, which reduces the risk of acute renal injury. The sensitivity of CT angiography is highest at a LE in the main pulmonary artery and the lobular and segmental vessels. The sensitivity of CT angiography is lowest at embolism in subsegmental vessels (about 30% of all LEs). However, the sensitivity and specificity of CT angiography have improved in the frame as the technology has developed. Pulmonary embolism (CT angiography) with permission of the publisher. From Kucher N., Goldhaber S., J. Sewell, et al. In Bone’s Atlas of Pulmonary and Critical Care Medicine. Edited by J. Crapo. Philadelphia, Current Medicine, 2005. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/pulmonary_embolism_helical_ct_scan_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / manual / professional / images / pulmonary_embolism_helical_ct_scan_high_de.jpg lang = en & thn = 0 ‘, title:’? pulmonary embolism (CT angiography) ‘description:’ u003Ca id = “v38395487 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eEin CT angiogram with multiple emboli on both sides u003c / p u003e u003c / div u003e. ‘credits’ with permission of the publisher. From Kucher N.