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Pulmonary embolism
A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venousthrombus, becomes dislodged from its site of formation and embolizesto the arterialblood supply of one of the lungs. Symptoms may include difficulty breathing, pain during breathing, and more rarely circulatory instability and death. Treatment is with anticoagulantmedication, such as warfarin.
Signs, symptoms and risk factorsClinical presentationSigns of PE are sudden-onset dyspnea(shortness of breath, 73%), tachypnea(rapid breathing, 70%), chest painof "pleuritic" nature (worsened by breathing, 66%), cough(37%), hemoptysis(coughing up blood, 13%), and in severe cases, cyanosis, tachycardia(rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosisin the legs, findings that indicate this may aid in the diagnosis. Risk factorsThe most common sources of embolism are proximal leg deep venous thrombosis(DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs. Risk factors for DVT and PE (together "venous thromboembolism" or VTE) can be divided into genetic, acquired and circumstantial causes. In many occasions, more than one risk factor is present:
DiagnosisConfirming pulmonary embolismThe gold standardfor diagnosing pulmonary embolism (PE) is pulmonary angiography. In most cases, however, when PE is suspected on the basis of shortness of breath and chest pain, the following studies may confirm the presence of an embolus. Pulmonary angiography is used less often because of wider acceptance of CT scans which are non-invasive.
In low/moderate suspicion of PE, a normal D-dimerlevel (shown in a blood test) is enough to exclude the possibility of PE (Bounameaux et al 1994). An electrocardiogrammay show signs of right heart strain or acute cor pulmonalein cases of large PEs - the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III ("S1Q3T3", as described by McGinn & White 1935). This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has therefore limited diagnostic value; The most commonly seen sign in the ECG is sinus tachycardia. In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary arteryis severely obstructed and the heart is unable to match the pressure. In the United States, many physicians see this as an adequate indication for thrombolysis(see below). The presence of deep venous thrombosisis in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans, and leg ultrasoundcan be used as a surrogate. This may be valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having pulmonary embolism. Further analysisWhen a PE is being suspected, a number of blood testsare also done, in order to exclude important secondary causes of PE. This includes a full blood count, clotting status(PT, APTT, TT), and some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted. TreatmentAcutely, supportive treatments, such as oxygenor analgesia, are often required. Massive PE causing hemodynamic instability (marked decreased oxygen saturation, tachycardiaand/or hypotension) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. Some advocate its use also if right ventricular dysfunction can be demonstrated on echocardiography(see e.g. Goldhaber 2004). In most cases, anticoagulanttherapy is the mainstay of treatment. Heparin, low molecular weight heparins, or fondaparinuxis administered initially, while warfarintherapy is commenced (this may take several days, usually while the patient is in hospital). Warfarin therapy is usually continued for 3-6 months, or "lifelong" if there have been previous DVTs or PEs, or none of the usual risk factors is present. Warfarin therapy often requires frequent dose adjustment and monitoring of the INR. In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5-3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. low molecular weight heparin. In patients with an underlying malignancy, therapy with a course of low molecular weight heparinmay be favored over warfarin based on the results of the CLOT trial (Lee et al, 2003). If anticoagulant therapy is contraindicatedand/or ineffective an inferior vena cava filtermay be implanted. PrognosisBefore anticoagulation became the accepted treatment, mortality from PE was about 26% (Baritt & Jordan 1960). Prognosis depends on the amount of lung that is affected and on the co-existence of other debilitating conditions. Chronic embolisation to the lung can lead to pulmonary hypertension. After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulanttherapy, a further search for underlying conditions is undertaken. This will include testing (see above for full list) for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulationabnormalities. HistoryAfter a trial published in 1960(Baritt & Jordan), anticoagulation became the most important therapeutic intervention in pulmonary embolism. Barritt and Jordan performed their study in the Bristol Royal Infirmaryin 1957. This study rapidly set the pace, considering that no other study of anticoagulation in PE ever had a placebo group (as this would have been unethical). Looking back, the reported mortality rate of 26% may have been an overstatement, given the fact that with the technology of the day, only severe PEs were detected. One notable victim of pulmonary embolism was William II, the last Kaiserof Germany. References
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de:Lungenembolie ko:폐색전증 es:Tromboembolismo pulmonar it:Embolia polmonare pt:Embolia pulmonar
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