Pulmonary embolus ( PE ) is the blockage of arteries in the lungs by substances that have moved from elsewhere in the body through the bloodstream (emboli). PE symptoms may include shortness of breath, chest pain especially when breathing, and coughing up blood. Symptoms of blood clots in the legs can also appear like red feet, warm, swollen, and pain. The signs of PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes mild fever. Severe cases can lead to fainting, abnormally low blood pressure, and sudden death.
PE usually results from blood clots in the legs that move into the lungs. The risk of blood clots is increased due to cancer, resting in old beds, smoking, stroke, certain genetic conditions, estrogen-based drugs, pregnancy, obesity, and after some surgery. A small number of cases are caused by air, fat, or amniotic fluid embolization. The diagnosis is based on signs and symptoms combined with the test results. If the risk is low, a blood test known as a D-dimer will rule out the condition. Otherwise, CT pulmonary angiography, lung/perfusion venous scan, or ultrasound in the legs may confirm the diagnosis. Together deep vein thrombosis and PE are known as venous thromboembolism (VTE).
Efforts to prevent PE include starting as soon as possible after surgery, lower leg exercises during the sitting period, and the use of blood thinners after some type of surgery. Treatment is usually with blood thinners such as heparin or warfarin. Often this is recommended for six months or longer. Severe cases may require thrombolysis using drugs such as tissue plasminogen activator (tPA), or may require surgery such as pulmonary thrombectomy. If the blood thinner is not appropriate, the vena cava filter can be used.
Pulmonary embolism affects approximately 430,000 people annually in Europe. In the United States between 300,000 and 600,000 cases occur each year, which results in between 50,000 and 200,000 deaths. Prices are similar in men and women. They become more common with age.
Video Pulmonary embolism
Signs and symptoms
Symptoms of pulmonary embolism are usually abrupt in onset and may include one or more of the following: dyspnea, tachypnea, chest pain due to "pleuritic" (worsening breathing), coughing and hemoptysis (coughing up). More severe cases may include signs such as cyanosis (blue discoloration, usually on the lips and fingers), collapse, and circulatory instability due to decreased blood flow through the lungs and to the left side of the heart. About 15% of all sudden death cases are caused by PE.
On physical examination, the lungs are usually normal. Occasionally, friction of pleural friction can be heard in the affected lung area (mostly in PE with infarction). Pleural effusions are sometimes exudative, detected by decreased percussion records, audible breath sounds, and vocal resonance. Tension in the right ventricle can be detected as the left parasternal heave, the lung component loud from the second heart sound, and/or increased jugular venous pressure. A mild fever may occur, especially if there is pulmonary bleeding or pulmonary infarction.
Because smaller pulmonary embolos tend to be in more peripheral areas without collateral circulation, they are more likely to cause pulmonary infarction and small effusions (both painful), but not hypoxia, dyspnea or hemodynamic instability such as tachycardia. Larger PE, which tends to be centralized, usually causes dyspnea, hypoxia, low blood pressure, rapid heartbeat and fainting, but is often painless because there is no pulmonary infarction due to collateral circulation. The classical presentation for PE with pleuritic pain, dyspnea and tachycardia may be caused by large fragmented emboli causing large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without other findings and large PEs are often missed because they do not cause pain and mimic other conditions that often cause ECG changes and small increases in troponin levels and BNP.
PE is sometimes described as massive, submasif and nonmassive depending on clinical signs and symptoms. Although the exact definition of this is unclear, the accepted large PE definition is one where there is hemodynamic instability such as sustained low blood pressure, slowing heart rate, or pulse rate.
Maps Pulmonary embolism
Risk factors
Approximately 90% of embolism is derived from deep vein thrombosis in the proximal leg (DVT) or pelvic venous thrombosis. DVT is at risk for uprooting and migrating to the pulmonary circulation. This condition is generally regarded as a series called venous veins (VTE).
The development of thrombosis is classical because of a group of causes called Virchow's triads (changes in blood flow, factors in blood vessel walls and factors affecting blood properties). Often, more than one risk factor is present.
- Changes in blood flow : immobilization (after surgery, long-haul flights), injury, pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)
- Factors in blood vessel wall : surgery, catheterization causing direct injury ("endothelial injury")
- Factors affecting blood properties (procoagulant status):
- Estrogen-containing hormonal contraceptives
- Genetic thrombophilia (factor V Leiden, prothrombin G20210A mutation, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders)
- Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)
- Cancer (due to pro-coagulant secretion)
Underlying cause
After the first PE, the search for secondary causes is usually short. Only when the second PE occurs, and especially when this occurs while still in anticoagulant therapy, further search for underlying conditions is performed. This will include testing ("thrombophilia screen") for Factor V Leiden mutations, antiphospholipid antibodies, protein C and S and antithrombin levels, and prothrombin mutations later, MTHFR mutations, Factor VIII concentrations and inherited coagulation abnormalities.
Diagnosis
To diagnose pulmonary embolism, a review of clinical criteria to determine the need for testing is recommended. In those with a low risk, age less than 50, heart rate less than 100 beats per minute, oxygen levels of more than 94% in room air, and no swelling of the feet, coughing up blood, surgery or trauma in the last four weeks, blood clots before, or estrogen use, further testing is usually not necessary.
If any of these concerns are followed by testing to determine the likelihood of being able to confirm the diagnosis by imaging, followed by imaging if other tests indicate that there is a possibility of a PE diagnosis.
The PE diagnosis is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) is indistinguishable from other causes of chest pain and shortness of breath. The decision to conduct medical imaging is based on clinical reasoning, ie medical history, symptoms and findings on physical examination, followed by clinical probability assessment.
Testing possibilities
The most common method used to predict clinical probabilities, the Wells score, is a clinical prediction rule, whose use is complicated by several available versions. In 1995, Philip Steven Wells, originally developed a prediction rule (based on literature search) to predict the probability of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during validation by Wells et al. in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs 2 or 4 with the same prediction rules. In 2001, Wells published the results using a more conservative cutoff of 2 to create three categories. The extended version, "extended extended version", uses the latest cutoff of 2 but includes findings from Wells's proposed initial study. Recently, further research goes back to the use of Wells from a 4 point cutoff to create just two categories.
There are additional prediction rules for PE, such as the Geneva rules. More importantly, the use of each rule is associated with a reduction in recurrent thromboembolism.
Wells Score :
- DVT clinical suspicion - 3.0 points
- alternative diagnosis is less likely than PE - 3.0 points
- tachycardia (heart rate & gt; 100) - 1.5 points
- immobilization (> = 3d)/operations in the previous four weeks - 1.5 points
- history of DVT or PE - 1.5 points
- hemoptysis - 1.0 points
- malignancy (with treatment within six months) or palliative - 1.0 points
Traditional interpretation
- Score & gt; 6.0 - High (possibly 59% based on collected data)
- Score 2.0 to 6.0 - Medium (29% probability based on collected data)
- Score & lt; 2.0 - Low (15% probability based on collected data)
Alternative interpretation
- Score & gt; 4 - PE possible. Consider diagnostic imaging.
- Score 4 or less - PE is not possible. Consider D-dimer to override PE.
Recommendations for diagnostic algorithms published by PIOPED researchers; However, this recommendation does not reflect the study using 64 MDCT slices. These researchers recommend:
- Clinical probability is low. If the D-dimer is negative, PE is excluded. If the D-dimer is positive, get MDCT and care based on results.
- Moderate clinical probability. If the D-dimer is negative, PE is excluded. However , I do not worry that MDCT negative with negative D-dimer in this setting has 5% chance of being wrong. Presumably, the 5% error rate will drop because 64 MDCT slices are more commonly used. If the D-dimer is positive, get MDCT and care based on results.
- High clinical probability. Continue to MDCT. If positive, treat, if negative, more tests are needed to exclude PE. D-dimers less than 750 ug/L do not rule out PE in those at high risk.
Criteria for the delivery of pulmonary embolism
The criteria for pulmonary embolism paralysis (PERC) help assess people suspected of pulmonary embolism, but it is not possible. Unlike the Wells score and the Geneva score, which is a clinical prediction rule intended to risk stratification of people with alleged PE, PERC rules are designed to rule out PE risk to people when doctors have grouped them into low risk categories.
People in this low risk category without these criteria may not undergo further testing for PE: low oxygen saturation - Sa O 2 & lt; 95%, unilateral leg swelling, cough blood, previous DVT or PE, surgery or new trauma, age & gt; 50, hormone use, rapid heartbeat. The reason behind this decision is that further testing (especially CT angiogram on the chest) may cause more damage (from radiation exposure and contrast dye) than the risk of PE. The PERC rule has a sensitivity of 97.4% and a specificity of 21.9% with a false negative rate of 1.0% (16/1666).
Blood tests
In people with low or moderate PE suspicion, normal D-dimer levels (shown in blood tests) are sufficient to rule out the possibility of thrombotic PE, with a three-month risk of thromboembolic incidence to 0.14%. D-dimers are very sensitive but not specific (specificity is about 50%). In other words, the positive D-dimer is not the same as the PE, but the D-dimer is negative, with a good degree of certainty, an indication of the absence of PE. The typical cut is 500 g/L, although this varies based on the test. However, in those over the age of 50, change the cut-off value to a person's age multiplied by 10? G/L (accounting for testing that has been used) is recommended because it reduces the number of false positive tests without the loss of additional PE cases.
When PE is under suspicion, some blood tests are performed to exclude an important secondary cause of PE. These include full blood count, clotting status (PT, aPTT, TT), and some screening tests (rate of sedimentation of blood, kidney function, liver enzyme, electrolyte). If any of these are not normal, further investigation may be required.
The troponin level increases between 16-47% with pulmonary embolism.
Imaging
In typical persons not known to be at high risk of PE, imaging is helpful for confirming or excluding PE diagnoses after a simpler first-line test is used. Medical societies recommend tests such as D-dimers to first provide supporting evidence for imaging needs, and imaging will be performed if other tests confirm a moderate or high probability to find evidence to support PE diagnosis.
CT pulmonary angiography is the first diagnostic imaging test recommended in most people.
Historically, the gold standard for diagnosis was pulmonary angiography, but this has become unused with the increasing availability of noninvasive techniques. Ultrasound on the foot can confirm the presence of PE but can not rule it out.
CT pulmonary angiography
CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained by computed tomography (CT) with radiocontrast rather than right heart catheterization. The advantages are clinical equality, noninvasive nature, greater availability in people, and the possibility of identifying other lung disorders from differential diagnosis if there is no pulmonary embolism.
Assessing the accuracy of CT pulmonary angiography is blocked by rapid changes in the number of detector lines available on multidetector CT (MDCT) machines. According to a cohort study, a one-slice spiral CT may help diagnose detection among people suspected of pulmonary embolism. In this study, the sensitivity was 69% and the specificity was 84%. In this study, the prevalence of detection was 32%, the positive predictive value of 67.0% and the negative predictive value of 85.2%. However, the results of this study may be biased due to possible merging bias, since CT scan is the ultimate diagnostic tool in people with pulmonary embolism. The authors note that CT scans of single negative slices are not sufficient to exclude pulmonary embolism by themselves. A separate study with a mixture of 4 slices and 16 slice scanners reported 83% sensitivity and 96% specificity, which means it is a good test to rule out pulmonary embolism if not seen in imaging and that is excellent in confirming pulmonary embolism present when seen. The study noted that additional testing is required when clinical probabilities are inconsistent with the results of the imaging. CTPA is not inferior to VQ scanning, and identifies more emboli (without increasing yield) than VQ scanning.
Ventilation/perfusion scan
Ventilation/perfusion scans (or V/Q scans or pulmonary scintigraphy) show that some areas of the lung are being ventilated but not blood-dipped (due to obstruction by clots). This type of examination is as accurate as CT multislice, but it is poorly used, due to the greater availability of CT technology. This is especially useful in people who have allergies to iodinated contrast, impaired renal function, or being pregnant (due to lower exposure to radiation compared with CT). This test can be performed with planar two-dimensional imaging, or single photon emission tomography (SPECT) that enables three-dimensional imaging. The hybrid device incorporating SPECT and CT (SPECT/CT) further allows characterization of the anatomy of any abnormality.
Low-probability diagnostic test/non-diagnostic test
Frequent tests are not sensitive to PE, but can be diagnostic.
- Chest x-rays are often performed on people with shortness of breath to help rule out other causes, such as congestive heart failure and rib fractures. Chest X-ray in PE is rarely normal, but usually there is no sign indicating PE diagnosis (eg, Westermark sign, Hampton hump).
- Foot ultrasound, also known as doppler leg, for deep venous thrombosis (DVT). The presence of DVT, as shown in foot ultrasonography, is self-sufficient to ensure anticoagulation, without the need for V/Q or spiral CT scans (due to the strong relationship between DVT and PE). This may be a valid approach in pregnancy, where other modalities will increase the risk of birth defects in unborn babies. However, a negative scan does not rule out PE, and a low radiation dose scan may be necessary if the mother is considered at high risk for pulmonary embolism. The main use of ultrasonography in the legs is in those who have clinical symptoms that lead to deep vein thrombosis.
Electrocardiogram
The main use of EKG is to rule out other causes of chest pain. Electrocardiogram (EKG) is routinely performed in people with chest pain to rapidly diagnose myocardial infarction (heart attack), an important differential diagnosis in individuals with chest pain. While certain ECG changes may occur with PE, none are specific enough to confirm or are sensitive enough to rule out the diagnosis. An ECG may show signs of a right heart strain or acute cor pulmonale in a large PE case - the classic mark is a large S wave at lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3), which occurs in 12-50% of people with diagnosis, but also occur in 12% without diagnosis.
It is occasionally present (occurring in up to 20% of people), but may also occur in other acute lung conditions, and therefore, has limited diagnostic value. The most common signs seen in ECG are sinus tachycardia, right axis distortion, and right bundle branch block. Sinus tachycardia, however, is still only found in 8-69% of people with PE.
The ECG findings associated with pulmonary embolism may show a poorer prognosis because six findings identified with the RV strain on ECG (heart rate & gt; 100 beats per minute, S1Q3T3, inverted T wave on V1-V4 lead, ST elevation in aVR, complete right block bundle block, and atrial fibrillation) are associated with an increased risk of circulatory shock and death.
Echocardiography
In massive and submasifive PE, dysfunction on the right side of the heart can be seen in echocardiography, an indication that the pulmonary artery is severely inhibited and the right ventricle, the low pressure pump, can not match the pressure. Several studies (see below) suggest that these findings may be indicative for thrombolysis. Not every person with pulmonary embolism (suspected) requires an echocardiogram, but elevated cardiac troponins or natriuretic peptides of the brain may indicate a heart strain and require an echocardiogram, and are important in prognosis.
The special appearance of the right ventricle in echocardiography is referred to as the McConnell sign . This is the finding of akinesia from the free mid-wall but the normal movement of the apex. This phenomenon has a sensitivity of 77% and a specificity of 94% for the diagnosis of acute pulmonary embolism in the setting of right ventricular dysfunction.
Prevention
Pulmonary embolism may be prevented in those with risk factors. Hospitalized people may receive preventive medications, including unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux, and anti-thrombosis stockings to reduce the risk of DVT in the legs that can excrete and migrate to the lungs.
After the completion of warfarin in those with prior PE, long-term aspirin is useful to prevent recurrence.
Treatment
Anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, may be necessary. People are often hospitalized in the early stages of treatment, and tend to remain in inpatient care until INR has reached therapeutic levels. Increasingly, however, low-risk cases are managed at home in a way that is already common in the treatment of DVT. The evidence to support one approach versus the other is weak.
Anticoagulation
Usually, anticoagulant therapy is the mainstay of care. Unfractionated heparin (UFH), low molecular weight heparin (LMWH), or fondaparinux are administered initially, while warfarin, acenocoumarol, or phenprocoumon therapy is initiated (this may take several days, usually when the patient is in hospital). LMWH may reduce bleeding among people with pulmonary embolism compared with UFH according to a systematic review of a randomized controlled trial by Cochrane Collaboration. According to the same review, LMWH reduces the incidence of recurrent thrombotic complications and reduces thrombus size when compared with heparin. There was no difference in overall mortality between participants treated with LMWH and those treated with unfractionated heparin.
Warfarin therapy often requires frequent dose adjustments and monitoring of international normalized ratios (INR). In PE, INR between 2.0 and 3.0 is generally considered ideal. If other PE episodes occur under warfarin treatment, the INR window may be increased to eg. 2.5-3.5 (unless there is contraindication) or anticoagulation may be converted into different anticoagulants eg. LMWH.
In patients with underlying malignancy, therapy with LMWH is preferred over warfarin; continued for six months, at which point decisions should be reached whether continuous care is needed.
Similarly, pregnant women are often maintained at low molecular weight heparin until at least six weeks after delivery to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy.
Warfarin therapy is usually continued for 3-6 months, or "lifetime" if there were previously DVT or PE, or no ordinary risk factors were present. Abnormal D-dimer levels at the end of treatment may signal the need for follow-up care among patients with an unpredictable pulmonary embolus first. For those with small PE (known as PE subsegmental) the anticoagulation effect is unknown because it has not been properly studied in 2014.
Thrombolysis
Massive PE causes hemodynamic instability (shock and/or low blood pressure, defined as systolic blood pressure & lt; 90 mmHg or 40 mmHg pressure drop for 15 minutes if not caused by new arrhythmias, hypovolemia or sepsis) is indicative for thrombolysis , enzymatic destruction of clots with drugs. In this situation, it is the best treatment available to those who are not contraindicated and supported by clinical guidelines. It is also recommended in those with cardiac arrest with known PE.
Thrombolysis directed by catheters (CDT) is a new technique found to be relatively safe and effective for large PEs. This involves accessing the venous system by placing the catheter into the blood vessels in the groin and guiding it through the blood vessels by using fluoroscopic imaging until it is located next to the PE in the pulmonary circulation. The drug that breaks the blood clot is released through the catheter so that the highest concentration is directly next to the pulmonary embolus. CDT is performed by intervention radiologists, and in medical centers offering CDT, may be offered as first-line treatment. Thrombolysis with the help of catheter-based ultrasonography is being investigated.
The use of thrombolysis in non-massive PE is debatable. Some have found that treatment reduces the risk of death and increases the risk of bleeding including intracranial haemorrhage. Others did not find a reduced risk of death.
Inferior vena cava filter
There are two situations when inferior vena cava filters are considered beneficial, and they are if anticoagulant therapy is contraindicated (eg immediately after major surgery), or a person has pulmonary embolus despite being anticoagulant. In this case, it may be implanted to prevent new or existing DVT from entering the pulmonary artery and combining with existing blockages. Apart from the theoretical advantages of devices to prevent pulmonary emboli, there is a lack of evidence to support its effectiveness.
Inferior vena cava filters should be removed as soon as it is safe to start using anticoagulation. Although modern filters are meant to be taken, complications can prevent some from being removed. The long-term safety profile of leaving the filter permanently inside the body is unknown.
Surgery
Surgical management of pulmonary pulmonary embolism (pulmonary thrombectomy) is rare and has largely been abandoned because of poor long-term outcomes. However, more recently, he has experienced a revival with revisions of surgical techniques and is considered beneficial to certain people. Chronic pulmonary embolism causing pulmonary hypertension (known as chronic thromboembolic hypertension ) is treated with a surgical procedure known as pulmonary thromboendarterectomy.
Epidemiology
Pulmonary embolism occurs in more than 600,000 people in the United States each year. This generates between 50,000 and 200,000 deaths per year in the United States. The risk in those admitted to hospital is about 1%. The rate of fatal pulmonary embolism has decreased from 6% to 2% over the last 25 years in the United States.
Prognosis
Less than 5 to 10% of symptomatic PE is fatal within the first hour of symptoms.
There are several markers used for risk stratification and this is also an independent predictor of adverse outcomes. These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevated cardiac enzymes. Some ECG changes including S1Q3T3 also correlate with a worse short-term prognosis. There are several other factors associated with patients such as COPD and chronic heart failure that also play a role in prognosis.
The prognosis depends on the number of lungs affected and on the coexistence of other medical conditions; Chronic embolization of the lungs may cause pulmonary hypertension. After a large PE, the embolus must be completed somehow if the patient wants to survive. In thrombotic PE, blood clots can be broken down by fibrinolysis, or may be organized and unalloyed so that new channels are formed through clots. The blood flow is restored most quickly on the first day or two after PE. Improvements slow down afterwards and some deficits may be permanent. There is controversy over whether small subsegmental PEs require treatment at all and some evidence exists that patients with subgroup PE may do well without treatment.
Once anticoagulation is stopped, the risk of fatal lung embolism is 0.5% per year.
Mortality from untreated PE is said to be 26%. This figure comes from an experiment published in 1960 by Barrit and Jordan, which compares anticoagulation to placebo for PE management. Barritt and Jordan conducted their studies at Bristol Royal Infirmary in 1957. This study was the only placebo-controlled trial ever to examine anticoagulant sites in PE treatment, a result so convincing that trials were never repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group may be excessive, given that the technology on that day may only detect severe PE.
Predicting mortality
PESI and SESSION assessment tools can estimate the patient's death. The Geneva prediction rules and Wells criteria are used to calculate the probability of a patient's pre-test to predict who has pulmonary embolism. This score is a tool to be used with clinical judgment in deciding on diagnostic tests and the type of therapy. The PESI algorithm consists of 11 clinically available variables on a regular basis. This places the subjects into one of five classes (I-V), with a 30-day mortality ranging from 1.1% to 24.5%. Those in grade I and II are at low risk and those in grade III-V are at high risk.
References
External links
- Pulmonary embolism in Curlie (based on DMOZ)
- Well criteria for online pulmonary embolism calculator
- Clinical prediction site - Wells criteria for pulmonary embolism
- Media related to pulmonary embolism on Wikimedia Commons
Source of the article : Wikipedia
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