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Pulmonary embolism
Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism). Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood. Symptoms of a blood clot in the leg may also be present, such as a red, warm, swollen, and painful leg. Signs of a PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes a mild fever. Severe cases can lead to passing out, abnormally low blood pressure, obstructive shock, and sudden death.
PE usually results from a blood clot in the leg that travels to the lung. The risk of blood clots is increased by advanced age, cancer, prolonged bed rest and immobilization, smoking, stroke, long-haul travel over 4 hours, certain genetic conditions, estrogen-based medication, pregnancy, obesity, trauma or bone fracture, and after some types of surgery. A small proportion of cases are due to the embolization of air, fat, or amniotic fluid. Diagnosis is based on signs and symptoms in combination with test results. If the risk is low, a blood test known as a D-dimer may rule out the condition. Otherwise, a CT pulmonary angiography, lung ventilation/perfusion scan, or ultrasound of the legs may confirm the diagnosis. Together, deep vein thrombosis and PE are known as venous thromboembolism (VTE).
Efforts to prevent PE include beginning to move as soon as possible after surgery, lower leg exercises during periods of sitting, and the use of blood thinners after some types of surgery. Treatment is with anticoagulant medications such as heparin, warfarin, or one of the direct-acting oral anticoagulants (DOACs). These are recommended to be taken for at least three months. However, treatment using low-molecular-weight heparin is not recommended for those at high risk of bleeding or those with renal failure. Severe cases may require thrombolysis using medication such as tissue plasminogen activator (tPA) given intravenously or through a catheter, and some may require surgery (a pulmonary thrombectomy). If blood thinners are not appropriate or safe to use, a temporary vena cava filter may be used.
Pulmonary emboli affect about 430,000 people each year in Europe. In the United States, between 300,000 and 600,000 cases occur each year, which contribute to at least 40,000 deaths. Rates are similar in males and females. They become more common as people get older.
Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE. While PE may present with syncope (fainting), less than 1% of syncope cases are due to PE.
On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative (fluid that leaks out of blood vessels). This is detectable by decreased percussion note, audible breath sounds, and vocal resonance. The strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.
As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea, and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs are often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and brain natriuretic peptide levels.
PEs are sometimes described as massive, submassive, and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability. This is a cause of obstructive shock, which presents as sustained low blood pressure, slowed heart rate, or pulselessness.
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Pulmonary embolism
Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism). Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood. Symptoms of a blood clot in the leg may also be present, such as a red, warm, swollen, and painful leg. Signs of a PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes a mild fever. Severe cases can lead to passing out, abnormally low blood pressure, obstructive shock, and sudden death.
PE usually results from a blood clot in the leg that travels to the lung. The risk of blood clots is increased by advanced age, cancer, prolonged bed rest and immobilization, smoking, stroke, long-haul travel over 4 hours, certain genetic conditions, estrogen-based medication, pregnancy, obesity, trauma or bone fracture, and after some types of surgery. A small proportion of cases are due to the embolization of air, fat, or amniotic fluid. Diagnosis is based on signs and symptoms in combination with test results. If the risk is low, a blood test known as a D-dimer may rule out the condition. Otherwise, a CT pulmonary angiography, lung ventilation/perfusion scan, or ultrasound of the legs may confirm the diagnosis. Together, deep vein thrombosis and PE are known as venous thromboembolism (VTE).
Efforts to prevent PE include beginning to move as soon as possible after surgery, lower leg exercises during periods of sitting, and the use of blood thinners after some types of surgery. Treatment is with anticoagulant medications such as heparin, warfarin, or one of the direct-acting oral anticoagulants (DOACs). These are recommended to be taken for at least three months. However, treatment using low-molecular-weight heparin is not recommended for those at high risk of bleeding or those with renal failure. Severe cases may require thrombolysis using medication such as tissue plasminogen activator (tPA) given intravenously or through a catheter, and some may require surgery (a pulmonary thrombectomy). If blood thinners are not appropriate or safe to use, a temporary vena cava filter may be used.
Pulmonary emboli affect about 430,000 people each year in Europe. In the United States, between 300,000 and 600,000 cases occur each year, which contribute to at least 40,000 deaths. Rates are similar in males and females. They become more common as people get older.
Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE. While PE may present with syncope (fainting), less than 1% of syncope cases are due to PE.
On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative (fluid that leaks out of blood vessels). This is detectable by decreased percussion note, audible breath sounds, and vocal resonance. The strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.
As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea, and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs are often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and brain natriuretic peptide levels.
PEs are sometimes described as massive, submassive, and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability. This is a cause of obstructive shock, which presents as sustained low blood pressure, slowed heart rate, or pulselessness.