Pulmonary embolism

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Pulmonary thromboembolism

Pulmonary thromboembolism

pulmonary thromboembolism or pulmonary thromboembolism is a blockage of an artery in the lungs by a substance that has moved from another part of the body through the bloodstream (thrombus). Symptoms of a PE may include shortness of breath (dyspnea), chest pain, especially when inhaling, and coughing up blood (haemoptysis). Symptoms may also occur such as: a blood clot in the leg, a red, hot, swollen, and sore leg. Signs of PE include low oxygen levels in the blood, rapid breathing (tachypnea), rapid heart rate (tachycardia), and sometimes a mild fever. Severe cases can cause fainting, abnormally low blood pressure (hypotension), obstructive shock, and sudden death.

PET is usually the result of a blood clot in the leg, which travels to the lung. The risk of blood clots is increased with cancer, prolonged bed rest, smoking, stroke, certain genetic conditions, estrogen-based medications, pregnancy, obesity, and after some types of surgery. A small proportion of cases are due to embolization of air, fat, or amniotic fluid. Diagnosis is based on signs and symptoms in combination with test results, if risk is low a blood test known as D-dimer can rule out the condition, otherwise a CT with pulmonary angiography, pulmonary ventilation Doppler/perfusion scan, or ultrasound of the legs can confirm the diagnosis. Together, deep vein thrombosis and PE are known as venous thromboembolism (VTE).

Efforts to prevent PE include: moving around as soon as possible after surgery, lower leg exercises during periods of sitting, and use of blood thinners after some types of surgery. Treatment consists of anticoagulants such as heparin, warfarin or one of the direct-acting oral anticoagulants (DOACs), these are recommended for at least three months. Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (TPA) given intravenously or through a catheter, and some may require surgery (a pulmonary thrombectomy). If anticoagulants are not appropriate, a temporary vena cava filter can be used [16].

Pulmonary thromboembolism affects about 430,000 people each year in Europe, while in the United States, between 300,000 and 600,000 cases occur each year and at least 40,000 deaths are attributed to it. The rates are similar in men and women, although they become more common as people age and are associated with chronic degenerative diseases.

Signs and symptoms

Symptoms of pulmonary embolism are often sudden in onset and may include one or many of the following: dyspnea (difficulty breathing), tachypnea (rapid breathing), chest pain of a 'pleuritic' nature; (which is made worse 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 due to decreased blood flow through the lungs and to the left side of the heart. Approximately 15% of all sudden death cases are attributable to PTE. Although PE can present with syncope, less than 1% of syncope cases are due to syncope.

On physical exam, the lungs are usually normal. Occasionally, a pleural friction rub can be heard over the affected area of the lung (mainly in PTE with infarction). Sometimes there is a pleural effusion that is exudative, which is detectable by decreased percussion note, audible breath sounds, and vocal resonance. Right ventricular tension can be detected as a left parasternal rise, a loud pulmonary component of the second heart sound, and/or increased jugular venous pressure. There may also be a low-grade fever, particularly if there is associated pulmonary hemorrhage or infarction.

Because smaller pulmonary emboli tend to lodge 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 PTEs, which tend to be centrally located, usually cause dyspnea, hypoxia, low blood pressure, rapid heart rate, and fainting, but are often painless as there is no lung infarction due to collateral circulation. The classic presentation of PE with pleuritic pain, dyspnea, and tachycardia is probably due to a large fragmented emboli causing both large and small PEs. Thus, small TPEs are often missed as they cause pleuritic pain alone without any other findings and large PEs are often missed because they are painless and mimic other conditions that often cause ECG changes and small increases in troponin and brain natriuretic peptide levels.

PET can be described as massive, submissive, and non-massive based on 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, such as sustained low blood pressure, slow heart rate, or lack of pulse.

Risk factors

Approximately 90% of emboli are due to proximal deep vein thrombosis (DVT) of the leg or pelvic vein thrombosis. DVT is at risk of displacing and migrating into the pulmonary circulation. The conditions are generally considered as a continuum termed venous thromboembolism (VTE).

VTE is much more common in immunocompromised individuals, as well as in individuals with comorbidities including:

• Those who undergo orthopedic surgery in or below the hip without prophylaxis. This is due to immobility during or after surgery, as well as venous damage during surgery.
• Patients with pancreatic and colon cancer (other forms of cancer may also be factors, but these are the most common). This is due to the release of procoagulants.
• The risk of VTE is greater during diagnosis and treatment, but decreases in remission.
• Patients with high-grade tumors.
• Pregnant women. As the body stands in what is known as "hypercoagulability state", the risk of bleeding during childbirth decreases and is regulated by a greater expression of factors VII, VIII, X, Von Willebrand and fibrinogen.
• Those who take estrogen medication. The development of thrombosis is typically due to a group of causes called Virchow triad (alterations in blood flow, factors in the wall of the vessels and factors that affect the properties of the blood). Often, more than one risk factor is present.
• Blood flow alterations: immobilization (after surgery, long-distance flight), injury, pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)
• Factors on the glass wall: surgery and catheterisms that cause direct injury ("endothelial lesion").
• Factors that affect blood properties (procoagulant state): Drugs that contain estrogens (transgenous hormone therapy, hormonal therapy for menopause and hormonal contraceptives). Genetic thrombophilia (factor V Leiden, mutation of protrombin G20210A, protein C deficiency, protein S deficiency, antitrombin deficiency, hyperhomocysteinemia, and plasminogen/fibrinolysis disorders). Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, nocturnal paroxysmal hemoglobinuria)
• Cancer (due to the secretion of procoagulants).

Although most pulmonary embolisms are the result of proximal deep vein thrombosis (DVT) of the leg, there are still many other risk factors that can also result in a pulmonary embolism.

Risk factors

• Varicose veins caused by vascular damage
• Pulmonary hypertension
• Diabetes mellitus
• Traumatic hip fractures that immobilize the patient
• Joint fixation (mainly in the legs)

Underlying causes

After a first episode of PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this occurs while still on anticoagulation therapy, is a further search for underlying conditions undertaken. This will include testing ('thrombophilia screening') 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 coagulation abnormalities.

Diagnosis

To diagnose pulmonary embolism, a review of clinical criteria is recommended to determine the need for testing. In those at low risk, they are younger than 50 years old, have a heart rate less than 100 beats per minute, an oxygen level greater than 94% on room air, and no leg swelling, coughing up blood, surgery, or trauma to the body. past four weeks, previous blood clots, or estrogen use, no further testing is usually needed.

In situations with people at higher risk, more testing is needed. A CT pulmonary angiogram (CTPA) is the most recommended method for the diagnosis of pulmonary embolism due to its ease of administration and accuracy. Although a CTPA is preferred, other tests can also be done. For example, a lower limb proximal compression ultrasound (CUS) can be used. This is a test that is primarily used as a confirmatory test, which means that it confirms a previous test that shows the presence or suspicion of a pulmonary embolism. Based on a cross-sectional study, CUS tests have a sensitivity of 41% and a specificity of 96%.

If there are concerns, this is followed by tests to determine the probability that a diagnosis can be confirmed by imaging, followed by imaging if other tests have shown that there is a possibility of a PTE diagnosis.

The diagnosis of PE is primarily based on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath and chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to perform medical imaging is based on clinical reasoning, ie, medical history, symptoms, and physical examination findings, followed by an assessment of clinical probability.

Probability Test

The method commonly used to predict clinical probability is the Wells score, a clinical prediction rule whose use is complicated by the availability of multiple versions. In 1995, Philip Steven Wells initially developed a prediction rule (based on a 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 it was simplified during a validation by Wells et al. In 2000, In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001 Wells published results using the more conservative limit of 2 to create three categories. He proposed an additional version, the "modified extended version," which uses the more recent limit of 2, but includes the results of Wells's initial studies. More recently, a subsequent study reverted to Wells' earlier use of a 4-point cutoff to create only two categories.

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with a reduction in recurrent thromboembolism.

The Wells score

• Clinically suspected TVP - 3.0 points
• Alternative diagnosis is less likely than Embolia Pulmonar (EP): 3.0 points
• Tachycardia (heart rate  100) - 1,5 points
• Demobilization (≥ 3d) / surgery in the previous four weeks - 1,5 points
• History of TVP or EP - 1.5 points
• Hemoptisis - 1.0 points
• Malignity (with treatment within six months) or palliative - 1.0 points

Traditional interpretation:

• Score  6.0 - High (59 % probability according to grouped data)
• Tip from 2.0 to 6.0 - Moderate (29 % probability based on grouped data)
• Score ≤2.0 - Low (15% probability according to grouped data)

Alternative interpretation:

• Score  4 - EP probability. Consider obtaining diagnostic images.
• Score 4 or less - unlikely PE. Consider the D-dimer to rule out the PET.

Investigators from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) published recommendations for a diagnostic algorithm; however, these recommendations do not reflect research using 64-slice MDCT:Multidetector computed tomography. These researchers recommended:

• Low clinical probability

If D-dimer is negative, PE is excluded. If D-dimer is positive, obtain MDCT and base treatment on the results.

• Moderate clinical probability

If D-dimer is negative, PE is excluded. However, the authors were not concerned that a negative D-dimer negative MDCT in this setting had a 5% chance of being false. Presumably the 5% error rate will decrease as 64-slice MDCT is used more frequently. If D-dimer is positive, obtain MDCT and base treatment on the results.

• High clinical probability

Proceed with MDCT. If positive treat, if negative further testing is needed to exclude PET. A D-dimer of less than 750 μg/L does not rule out PE in those who are at high risk.

Criteria to rule out pulmonary embolism

Pulmonary embolism rule-out criteria (PERC) help evaluate people in whom pulmonary embolism is suspected but unlikely. Unlike the Wells score and the Geneva score, which are clinical prediction rules designed to risk stratify people with suspected PE, the PERC rule is designed to rule out PE risk in people when the doctor has already has stratified them into a low-risk category.

People in this low-risk category without any of these criteria may not undergo further PET testing: low oxygen saturation - SaO2 < 95%, unilateral leg swelling, coughing up blood, previous DVT or PE, recent surgery or trauma, age > 50, hormone use, rapid heart rate. The rationale for this decision is that additional tests (specifically CT angiography of the chest) may cause more harm (due to radiation exposure and contrast medium) 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 test

In people with a low or moderate suspicion of PE, a normal D-dimer level (shown on a blood test) is sufficient to exclude the possibility of thrombotic PE, with a risk of thromboembolic events at three months of 0.14%. D-dimer is highly sensitive, but not specific (specificity about 50%). In other words, a positive D-dimer is not synonymous with PE, but a negative D-dimer is, with a good degree of certainty, an indication of the absence of PE. A low pretest probability is also valuable in ruling out PE. The typical cut-off value is 500 μg/L, although it varies by assay. However, in people older than 50 years, it is recommended to change the cut-off value to the age of the person multiplied by 10 μg/L (taking into account the assay that has been used), since it reduces the number of false positive tests. without losing any additional evidence. PE cases.

When PE is suspected, several blood tests are done to rule out important secondary causes of PE. This includes a complete blood count, coagulation status (PT, aPTT, TT), and some screening tests (erythrocyte sedimentation rate, kidney function, liver enzymes, electrolytes). If one of these is abnormal, further investigation into it may be warranted.

Troponin levels are increased by 16-47% with pulmonary embolism.

Images

In typical people not known to be at high risk for PE, imaging is helpful in confirming or excluding a PE diagnosis after simpler first-line tests are used. Tests such as D-dimer are recommended by medical societies to first provide evidence to support the need for imaging, and imaging would be done if other tests confirmed a moderate or high probability of finding evidence to support a diagnosis of PD.

CT pulmonary angiography is the recommended first-line imaging test in most people.

Ultrasound of the legs can confirm the presence of PE, but cannot rule it out.

CT Pulmonary Angiography

CT pulmonary angiography (CTPA) is a pulmonary angiography obtained using radiocontrast computed tomography (CT) instead of catheterization of the right heart. Its advantages are that it is accurate, non-invasive, more commonly available, and can identify other lung disorders in the absence of pulmonary embolism. The precision and non-invasive nature of CTPA also make it advantageous for pregnant women.

Assessment of the accuracy of CT pulmonary angiography is hampered by rapid changes in the number of detector rows available on multidetector CT (MDCT) machines. According to a cohort study, single-slice spiral CT can help diagnose screening in people with suspected 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 67%, and the negative predictive value 85.2%. However, the results of this study may be biased due to possible incorporation bias, since computed tomography was the final diagnostic tool in people with pulmonary embolism. The authors noted that a negative single-slice CT scan is insufficient to rule out pulmonary embolism on its own. A separate study with a mix of 4-slice and 16-slice scans reported a sensitivity of 83% and a specificity of 96%, meaning it is a good test to rule out a pulmonary embolism if it is not seen on imaging and is very good for confirming that there is a pulmonary embolism if it is seen. This study pointed out that additional tests are needed when the clinical probability is inconsistent with the imaging results. CTPA is not inferior to the VQ scan and identifies more emboli (without necessarily improving outcome) compared to the VQ scan.

Ventilation/perfusion scan

Ventilation-perfusion scan

(A) After inhalation of 20 mCi of Xenon-133 gas, posterior projection scintigraphic images were obtained, showing uniform ventilation to the lungs.

(B) After intravenous injection of 4 mCi of technetium -99m labeled albumin, scintigraphic images shown here in posterior projection. This and other views showed decreased activity in several regions. A ventilation/perfusion scan (or V/Q scan or lung scan) shows that some areas of the lung are being ventilated, but not perfused with blood (due to clot obstruction). This type of exam is as accurate as multi-slice CT, but is less widely used due to the increased availability of CT technology. It is particularly useful in people who have an allergy to iodinated contrast medium, impaired kidney function, or are pregnant (because of its lower radiation exposure compared to CT). The test can be performed with flat two-dimensional imaging or with single photon emission computed tomography (SPECT) which allows three-dimensional imaging. Hybrid devices that combine SPECT and CT (SPECT/CT) also allow the anatomical characterization of any anomaly.

Diagnostic tests / low probability non-diagnostic tests

Frequently performed tests that are not sensitive to PET, but may be diagnostic.

• Chest X-rays are often performed in people with difficulty breathing to help rule out other causes, such as hypertensive heart disease with congestive heart failure and rib fracture. Chest X-rays in PET are rarely normal, but usually there are no signs suggesting the diagnosis of PET (e.g., Westermark sign, Hampton hump).
• Leg ultrasound, also known as leg doppler, in search of deep vein thrombosis (TVP). The presence of TVP, as shown in the ultrasound of the legs, is in itself sufficient to justify the anticoagulation, without requiring the V/Q or the CT scan in spiral (due to the strong association between TVP and TEP). This may be a valid approach to pregnancy, in which the other modalities would increase the risk of birth defects in the fetus. However, a negative scan does not rule out PET, and it is possible that a low-dose scan is required if the mother is considered to have a high risk of pulmonary embolism. Therefore, the main use of the ultrasound of the legs are those with clinical symptoms that suggest deep vein thrombosis.

Fluoroscopic Pulmonary Angiography

Historically, the gold standard for the diagnosis of PE was fluoroscopy pulmonary angiography, but this has fallen out of favor with the increased availability of noninvasive techniques that offer similar diagnostic accuracy.

EKG

The primary use of an electrocardiogram (EKG) is to rule out other causes of chest pain. An EKG is routinely performed on people with chest pain to quickly diagnose myocardial infarctions (heart attacks), Acute Coronary Syndromes (ACS), Angina, an important differential diagnosis in a person with chest pain. While certain EKG changes can occur with PET, none are specific enough to confirm or sensitive enough to rule out the diagnosis. An EKG may show signs of right heart distension or acute cor pulmonale in cases of large PE. 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), which occurs in 12-50% of people with the diagnosis, but it also occurs in 12% without diagnosis.

This is occasionally present (occurs in up to 20% of people), but can also occur in other acute lung conditions and is therefore of limited diagnostic value. The most common EKG findings are sinus tachycardia, right axis deviation, and right bundle branch block (RBBB). However, sinus tachycardia is still found in only 8 to 69% of people with PE.

EKG findings associated with pulmonary emboli may suggest a worse prognosis, as the six findings identified with RV tension on the EKG (heart rate > 100 beats per minute, S1Q3T3, inverted T waves in leads V1- V4, ST elevation in aVR, complete right bundle branch block (RBBB), and atrial fibrillation) are associated with increased risk of circulatory shock and death.

Cases with inverted T in leads V1-3 are suspected with PE or inferior or diaphragmatic myocardial infarction. TPE in some cases show inverted T waves in leads II and aVF, but inferior MI cases do not show inverted T waves in leads II and aVF.

Echocardiography

In massive and submassive PET, right-sided heart dysfunction can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the right ventricle, a low-pressure pump, cannot match the pressure. pressure. Some studies suggest that this finding may be an indication of thrombolysis. Not everyone with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate cardiac stress and warrant an echocardiogram, and be important in prognosis.

The specific appearance of the right ventricle on echocardiography is called McConnell's sign. This is the finding of median free wall akinesia, but normal apex movement. 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 can be prevented in people with risk factors. People admitted to the hospital may receive preventive medications, including unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux, and antithrombosis stockings to reduce the risk of a DVT in the leg that could dislodge and migrate to the lungs.

Once anticoagulation is completed in those with prior PE, long-term aspirin is helpful in preventing recurrence.

Treatment

Anticoagulant therapy is the mainstay of treatment. Acute supportive treatments, such as oxygen or analgesia, may be required. Often people are admitted to the hospital early in treatment and tend to remain under hospital care until the INR has reached therapeutic levels (if warfarin is used). However, increasingly, low risk cases are treated at home in a way that is already common in the treatment of Deep Vein Thrombosis. The evidence supporting one approach over the other is weak.

Anticoagulation

Anticoagulant therapy is the mainstay of treatment. For many years, vitamin K antagonists (warfarin or, less frequently, acenocoumarol or phenprocoumon) have been the cornerstone. Since vitamin K antagonists do not act immediately, initial treatment is with short-acting injectable anticoagulants: unfractionated heparin (UFH), low molecular weight heparin (LMWH), or fondaparinux, while vitamin K antagonists by orally are started and titrated (usually as part of hospitalization).
hospital care) to the international normalized ratio, a test that determines the dose.
As for injectable treatments, LMWH may reduce bleeding among people with pulmonary embolism compared to UFH.
According to the same review, ^[which?] LMWH reduced the incidence of recurrent thrombotic complications and reduced thrombus size compared with heparin. There was no difference in overall mortality between participants treated with LMWH and those treated with unfractionated heparin.^{[citation needed]}
Vitamin K antagonists require frequent dose adjustment and international normalized ratio (INR) monitoring. In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs with warfarin treatment, the INR window may be increased to, for example, 2.5-3.5 (unless there are contraindications),^{[citation needed]} anticoagulation can be changed to a different anticoagulant, eg LMWH.

In recent years, many anticoagulants have been introduced that offer a similar offering to warfarin, but without the need for INR adjustment. These treatments, known as direct-acting oral anticoagulants, are now preferred over vitamin K antagonists based on American professional guidelines. Two of these (rivaroxaban and apixaban) do not require initial treatment with heparin or fondaparinux, while dabigatran and edoxaban do. A Cochrane review found that there is no evidence of a difference between oral DTIs (dabigatran, rivaroxaban, edoxaban, apixaban) and standard anticoagulation in preventing recurrent pulmonary embolism.

In people with cancer who develop pulmonary embolism, therapy with a course of LMWH is preferred over warfarin or other oral anticoagulants. Similarly, pregnant women are treated with low molecular weight heparin until after delivery to avoid the known teratogenic effects of warfarin, especially in early pregnancy, but it can be used during lactation.

Anticoagulation therapy is usually continued for 3 to 6 months, or "for life" if there has been previous DVT or PE, or none of the usual transient risk factors are present. In those without a known cause that can be reversed, 2 years of treatment may be better than 6 months. For those with small PEs (known as subsegmental PEs) the effects of anticoagulation are unknown, as it has not been adequately studied as of 2020.

Thrombolysis

Massive PE causing hemodynamic instability (obstructive shock and/or low blood pressure, defined as a systolic blood pressure 15 min if not caused by arrhythmia, hypovolemia or new-onset sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. In this situation, it is the best available treatment in those without contraindications and is supported by clinical guidelines. It is also recommended in cardiac arrest patients with a known PE. Catheter-directed thrombolysis (CDT) is a new technique that has been found to be relatively safe and effective for massive PTE. This involves accessing the venous system by placing a catheter in a groin vein and guiding it through the veins using fluoroscopic imaging until it is located next to the PET in the pulmonary circulation. The blood clot-dissolving drug is delivered through the catheter so that its highest concentration is directly next to the pulmonary embolism. CDT is performed by interventional radiologists or vascular surgeons, and in medical centers that offer CDT, it may be offered as first-line treatment. Catheter-based ultrasound-assisted thrombolysis is being investigated.

The use of thrombolysis in non-massive PTE is still debated. Some have found that treatment reduces the risk of death and increases the risk of bleeding, including intracranial bleeding. Others have not found a decreased risk of death.

Inferior vena cava filter

There are two situations in which an inferior vena cava filter is considered advantageous and they are if anticoagulant therapy is contraindicated (for example, shortly after a major operation) or if a person has a pulmonary embolism despite being on anticoagulation. In these cases, it can be implanted to prevent new or existing DVTs from entering the pulmonary artery and combining with an existing blockage. Despite the theoretical advantage of the device in preventing pulmonary embolism, 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 anticoagulants. Although modern filters are meant to be salvageable, complications can prevent some from being removed. The long-term safety profile of permanently leaving a filter inside the body is unknown.

Surgery

Surgical treatment of acute pulmonary embolism (pulmonary thrombectomy) is rare and has been largely abandoned due to poor long-term outcomes. However, it has recently experienced a resurgence with revision of the surgical technique and is believed to benefit certain individuals. Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Epidemiology

There are approximately 10 million cases of pulmonary embolisms each year. In the United States, pulmonary embolism is the leading cause of at least 10,000 to 12,000 deaths per year and a contributing cause in at least 30,000 to 40,000 deaths per year. The true incidence of pulmonary emboli is unknown because they are often undiagnosed or unrecognized until autopsy. From 1993 to 2012, there has been an increase in the number of hospital admissions due to pulmonary embolism, from 23 cases per 100,000 people to 65 cases per 100,000 people. Despite this increase, there has been a decrease in mortality during that same time period due to the medical advances that have occurred.

Venous thromboembolism (VTE), a common risk factor, occurs at much higher rates in people older than 70 years (three times higher compared to people 45 to 69 years). This is probably because there is a generally lower activity level among the elderly, resulting in higher rates of immobility and obesity. VTE has a large and constantly increasing case fatality rate. This rate is approximately 10% after 30 days, 15% after three months, and up to 20% after one year. Pulmonary emboli alone (when they result in hospitalizations) have a case fatality rate of about 5% to 10%, so VTE may play an important factor in the severity of emboli.

Looking at all cases, the rate of fatal pulmonary emboli has decreased from 6% to 2% over the past 25 years in the United States. In Europe, an average of approximately 40,000 deaths per year with pulmonary embolism as the main cause were reported between 2013 and 2015, a conservative estimate due to possible underdiagnosis.

Forecast

Less than 5 to 10% of symptomatic pulmonary embolisms (PE) are fatal within the first hour of symptoms. There are several markers that are used for risk stratification and these are also independent predictors of adverse outcomes. These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevation of cardiac enzymes. Some ECG changes, including the S1Q3T3, also correlate with a worse short-term prognosis. There have been other patient-related factors, such as COPD and chronic heart failure, that are thought to influence prognosis as well.

The prognosis depends on the amount of lung affected and the coexistence of other medical conditions. Chronic embolization in the lung can lead to pulmonary hypertension. After a massive PTE, the embolism must somehow resolve for the patient to survive. In thrombotic PTE, the blood clot can be broken down by fibrinolysis, or it can be organized and recanalized so that a new channel is formed through the clot. Blood flow returns more quickly in the first day or two after a TEP. Improvement slows thereafter and some deficits may be permanent. There is controversy as to whether small subsegmental PEs need treatment and there is some evidence that patients with subsegmental PEs may do well without treatment.

Once anticoagulation is stopped, the risk of fatal pulmonary embolism is 0.5% per year.

Untreated PET mortality was said to be 26%. This figure comes from an essay published in 1960 by Barrit and Jordan, which compared placebo anticoagulation for the treatment of PET. Barritt and Jordan conducted their study at the Bristol Royal Infirmary in 1957. This study is the only placebo-controlled trial that has examined the place of anticoagulants in the treatment of PET, whose results were so compelling that the trial has never been repeated, as doing so would be considered unethical. That said, the reported mortality rate of 26 % in the placebo group is probably an exaggeration, since the technology of the moment may have detected only severe PET.^{[chuckles]required]}

Predict mortality

The PESI and sPESI scoring tools can estimate patient mortality. The Geneva prediction rules and Wells criteria are used to calculate a pretest probability of patients to predict who has a pulmonary embolism. These scores are tools that will be used with clinical judgment to decide diagnostic tests and types of therapy. The PESI algorithm comprises 11 routinely available clinical variables. It places subjects into one of five classes (I–V), with 30-day mortality ranging from 1.1% to 24.5%. Those in classes I and II are low risk and those in classes III-V are high risk.

The risk of mortality is determined by the acute dysfunction of the right ventricle, this can be evidenced by clinical, laboratory, and computed tomography and echocardiogram studies.

Mortality varies widely depending on the clinical severity of the embolism and ranges from 1% to more than 50%.